akshay. p. bavikatte 2012
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“CLINICOPATHOLOGICAL STUDY OF
SALIVARY SWELLINGS”
BY
Dr. AKSHAY. P. BAVIKATTE
M.B.B.S.,
Dissertation submitted to the
Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore.
In Partial fulfillment
Of the requirement for the degree of
MASTER OF SURGERY IN
GENERAL SURGERY
Under the guidance of
Dr. R.L.CHANDRASHEKAR M.S.,
Professor and
Head of the Department
DEPARTMENT OF GENERAL SURGERY
J.J.M. MEDICAL COLLEGE
DAVANGERE – 577 004.
2012
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ACKNOWLEDGEMENT It is most appropriate that I begin by expressing my undying gratitude to the
ALMIGHTY GOD for giving me the strength both mentally and physically to
complete this task.
It gives me great pleasure in preparing this dissertation and I take this
opportunity to thank everyone who have made this possible.
“First and foremost I would like to express my deep gratitude and sincere
thanks to my guide Dr. R.L. CHANDRASHEKAR M.S., Professor and HOD,
Department of General Surgery , J.J.M. Medical College, Davangere, for preparing
me for this task, guiding me with his superb talent and professional expertise,
showing great care and attention to details and without his supervision and guidance
this dissertation would have been impossible”.
I am highly indebted to Dr. R.L. CHANDRASEKHAR,M.S., Professor
and Head of the Department of General Surgery, J.J.M. Medical College,
Davangere, for his invaluable guidance. My special thanks and gratitude to my
professors Dr. M. SHIVKUMAR, Dr. G.C. RAJENDRA, Dr. SHUBHA RAO,
Dr. DINESH M.G., Dr. J.T. BASAVARAJ, Dr. S.N. SOMASEKHAR, Dr.
MANJUNATH GOWDA, Dr. U. MAHENDRANATH PATIL, Dr. DEEPAK G.
UDAPUDI, Dr. B.V.C. JAGADEESH, Dr. M.C. ANUPKUMAR, Dr.
RUDRAIAH H.G., Dr. VIRUPAXAGOWDA PATIL for their timely suggestions
and constant encouragement.
My special thanks to our Readers Dr. MAHESH.K., Dr. SUSRUTH
MARLAHALLI, Dr. PRAKASH.M.G. for their valuable advice and support.
I am thankful to Dr. K.C. SHIVMURTHY M.ch., Professor of Plastic Surgery,
Dr. H.B. SHIVKUMAR M.ch., Professor of Urology, Dr. C.J.
SHANTHKUMAR,M.ch., Professor of Neurosurgery, Dr.JAYALAKSHMIM.ch.,
Professor of Pediatric Surgery for their valuable help and support.
I would like to thank our Assistant Professors Dr. B.N. BASAVARAJ,
Dr. HARSHITH HEGDE, Dr. NATRAJ K.M., Dr. SHASHANK M.S., Dr.
PRADEEP for their valuable suggestions.
I also express my sincere thanks to Superintendents of Chigateri General
Hospital and Bapuji Hospital for allowing me to study the patients of their hospital.
I would like to express my sincere thanks to all the staff and pg students of
Department of Radio-diagnosis for helping out in the collection of data.
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LIST OF ABBREVATIONS USED
ACC : Acinic Cell Carcinoma
AdCC : Adenoid Cystic Carcinoma
BCA : Basal Cell Adenoma
C\S : Cut Section
CT : Computerised Tomography
FNAC : Fine Needle Aspiration Cytology
H\o : History Of
HPE : Histopathological Examination
MEC : Mucoepidermoid Carcinoma
MRI : Magnetic Resonance Imaging
PA : Pleomorphic Adenoma
RT : Radiotherapy
SCC : Squamous Cell Carcinoma
WT : Warthin’s Tumour
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ABSTRACT
BACKGROUND AND OBJECTIVES:
Salivary Gland swellings are one of the most common clinical conditions
encountered by the general surgeon. There are various causes of salivary swellings
and they arouse much interest and debate because of their remarkable variability in
structure, clinical presentation and behavior. Aggressive surgical resection is the
mainstay of the treatment of both benign and malignant salivary gland pathology.
This study was done with an interest to know the incidence, clinical presentation of
the non inflammatory and neoplastic swellings of the salivary glands and their
subsequent management and complications and to study the correlation of the FNAC
with the histopathology.
MATERIALS AND METHODS:
The present study is a time bound prospective study of forty consecutive cases
of salivary gland swellings admitted in various surgical units in J.J.M. Medical
College and Chigateri District hospital, Davangere, during the period from May 2009
to July 2011. Salivary gland swellings due to inflammatory conditions, salivary gland
swellings due to congenital conditions and salivary gland swellings due to systemic
conditions are excluded in order to more clearly define the study group. All patients
underwent pre- operative work up and surgery except for one patient who was
referred to kidwai memorial institute of oncology. Patients were referred to Kidwai
Memorial Institute of Oncology for post operative radiotherapy if needed. Follow up
period range from 3 months to 24 months. Data from 40 cases is presented here,
which were analyzed and conclusions drawn.
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RESULTS:
Salivary gland swelling occurred more commonly in 3rd and 4
th decades of life
(28.57%) and 65% of salivary swellings were present in females. All patients
presented with salivary gland swelling ( 100%) , 65% of patients presented with pain
and 55% of patients presented with tenderness .Among the non inflammatory and
neoplastic swellings, 65% of salivary swellings were neoplastic and 35% non
inflammatory swellings. Among non inflammatory swellings 80% was sialolithiasis
and 20% was ranula. 100% of sialolithiasis were present in submandibular salivary
glands. 100% of ranula was present in sublingual salivary glands. Among the
neoplastic swellings, 100% of the neoplastic swellings were present in parotid glands.
Benign tumors were common constituting 96.1% of salivary gland tumors.
Pleomorphic adenoma is the most common with 84.6%. The only malignant tumour
in the study is adenoid cystic carcinoma seen in only one case. FNAC has overall
diagnostic accuracy of 100%.Superficial parotidectomy is the most common surgery
performed for neoplastic lesions (56.41%). Excision of the submandibular salivary
gland is the most common surgery performed for non inflammatory swellings. Wound
infection is the most common post operative complications.
CONCLUSION:
Non-inflammatory and neoplastic salivary swellings are common in the
middle age group and in females. Neoplastic swellings are more common. Non-
inflammatory swellings are more common in submandibular salivary glands.
Sialolithiasis predominated the non- inflammatory swellings. Neoplastic swellings are
more common in parotid gland. pleomorphic adenoma dominates the neoplastic
swellings. FNAC has got a good accuracy in diagnosing salivary gland tumours. Plain
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X ray has got good accuracy in diagnosing sialolithiasis. Surgery is the main modality
in the treatment in both non inflammatory and neoplastic salivary gland swellings.
Early diagnosis of the condition with subsequent surgical management carries a very
good prognosis.
KEYWORDS: Parotid gland; Submandibular gland; sublingual gland; pleomorphic
adenoma; adenoid cystic carcinoma; superficial parotidectomy; excision of
submandibular salivary glands.
xii
TABLE OF CONTENTS
SL. No. PAGE No.
1 INTRODUCTION 1
2 OBJECTIVES 4
3 REVIEW OF LITERATURE 5
4 METHODOLOGY 136
5 RESULTS 139
6 DISCUSSION 154
7 CONCLUSION 158
8 SUMMARY 160
9 BIBLIOGRAPHY 163
10 ANNEXURES
ANNEXURE I: PROFORMA 176
ANNEXURE II: MASTER CHART 180
ANNEXURE III: CONSENT FORM 184
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LIST OF TABLES
TABLE
No. TABLES PAGE No.
1 Incidence of Salivary Gland Swellings at C.G. Hospital and
Bapuji Hospital 139
2 Age Distribution of Salivary Swellings 140
3 Sex Distribution 141
4 Mode of Clinical Presentation 142
5 Site for Various Salivary Gland Swellings 143
6 Various Causes of Salivary Swelling 144
7 Incidence of Non Inflammatory, Non- Neoplastic Swellings 145
8 Site Involvement in Non Inflammatory Non-Neoplastic
Swellings 146
9 Incidence of Benign and Malignant Salivary Gland
Tumours 147
10 Tumours Site and Side Distribution of Various Salivary
Gland 148
11 Incidence of Superficial and Deep Lobe Involvement of
Parotid Gland Tumours 149
12 Incidence of Various Salivary Glands Tumours 150
13 Correlation of FNAC and Histopathology 151
14 Surgical Procedures Adopted For Various Salivary Gland
Swellings
152
15 Post Operative Complications 153
16 Incidence Per Year of Salivary Gland Tumours in Different
Series
154
17 Incidence of Sialolithiasis in Various Studies 154
xiv
TABLE
No. TABLES PAGE No.
18 Frequency of Benign And Malignant Salivary Tumours in
Different Series
155
19 Location of Various Tumours in Different Series 155
20 Incidence of Superficial and Deep Lobe Involvement of
Parotid Gland Tumours in Different Series
156
21 Average Age Incidence of Salivary Gland Tumours in
different Series
156
22 FNAC Comparison with Pathologic Diagnosis in Different
Series
157
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LIST OF GRAPHS
GRAPH
No. GRAPHS
PAGE
No.
1 Age Distribution 140
2 Sex Distribution 141
3 Mode of Clinical Presentation 142
4 Site for Various Salivary Gland Swellings 143
5 Various Causes of Salivary Swelling 144
6 Incidence of Non Inflammatory, Non- Neoplastic Swellings 145
7 Site Involvement in Non Inflammatory Non-Neoplastic
Swellings
146
8 Incidence of Benign and Malignant Salivary Gland
Tumours
147
9 Tumours Site and Side Distribution of Various Salivary
Gland
148
10 Incidence of Superficial and Deep Lobe Involvement of
Parotid Gland Tumours
149
11 Incidence of Various Salivary Glands Tumours 150
12 Correlation of FNAC and Histopathology 151
13
Surgical Procedures Adopted for Various Salivary Gland
Swellings
152
14 Post Operative Complications 153
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LIST OF GRAPHS
FIGURE
No. FIGURES
PAGE
No.
1 Anatomy of salivary glands 11
2 The origin of salivary glands 13
3 Morphology of major salivary glands 15
4 Histology of the ductal system 15
5 Anatomical relations of parotid gland 23
6 Histology of parotid gland 23
7 Anatomy of submandibular salivary glands 26
8 Histology of submandibular salivary glands 27
9 Anatomy of sublingual salivary glands 29
10 Histology of submandibular salivary glands 29
11 Gross specimen of pleomorphic adenoma 47
12 Histopathology of pleomorphic adenoma 47
13 Gross specimen of warthin’s tumour 48
14 Histopathology of warthin’s tumour 48
15 Histopathology of basal cell adenoma 53
16 Histopathology of myoepithelioma 53
17 Histopathology of oncocytoma 54
18 Histopathology of canalicular adenoma 54
19 Gross specimen of acinic cell carcinoma 60
20 Histopathology of acinic cell carcinoma 60
21 Histopathology of adenoid cystic carcinoma 62
22 Histopathology of mucoepidermoid carcinoma 63
23 Photograph of oral salivary calculi 89
24 Photograph of left pleomorphic adenoma 89
25 Photograph of left submandibular sialolithiasis 90
26 Photograph of right pleomorphic adenoma with deep lobe
involvement with skin change and ear lobe elevation
90
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FIGURE
No. FIGURES
PAGE
No.
27 Photograph of left pleomorphic adenoma with ear lobe
elevation
91
28 Photograph showing mucous retention cyst in mouth 91
29 x-ray of submandibular calculi 98
30 Sialogram showing stricture of submandibular duct 98
31 Ultrasound showing warthin’s tumour 101
32 C T scan of mucoepidermoid carcinoma of right parotid 101
33 MRI of pleomorphic adenoma of left parotid 102
34 Photograph of modified blair incision 134
35 Photograph showing branches of facial nerve 134
36 Photograph showing deep lobe of parotid gland with facial
nerve
134
37 Excised specimen of pleomorphic adenoma of parotid gland 135
38 Photograph of wound closure of superficial parotidectomy 135
39 Photograph showing surgery of submandibular salivary
gland
135
1
INTRODUCTION
Salivary glands, major and minor, comprise a complex anatomic and
physiologic “organ” system-producing enzyme, lubrication, mixing agent and
immune factors. They may fall prey to a host of pathologic conditions including
infection, immune disorder, hypertrophy and atrophy, systemic disease and
“neoplastic both benign and malignant”1.
Salivary gland swellings can be broadly classified into inflammatory, non-
inflammatory and neoplastic swellings like calculi, benign tumours such as
pleomorphic adenoma, oncocytoma, warthin’s tumour or malignant tumours like
adenocarcinoma, adenoid cystic carcinoma and undifferentiated carcinoma.
Connective tissue diseases like haemangioma, lymphangioma, neurofibroma and
other auto immune diseases like Sjogren’s syndrome, Mikulicz disease etc2.
Acute inflammatory conditions generally can be diagnosed by history and
physical examination alone, whereas chronic inflammatory diseases and
granulomatous disorders require supplemental diagnostic information including lab
tests, imaging studies and biopsy. Accurate pathological diagnosis is necessary for
proper management of neoplastic disorders2.
About 64-80% of all primary epithelial tumours occur in parotid glands, 7-
11% in the submandibular glands, less than 1% in the sublingual glands and 9-23% in
the minor glands1. 15-30% of tumours in the parotid gland are malignant in contrast to
about 40% in the submandibular gland, 50% in the minor salivary gland and 70-90%
of sublingual glands3. The ratio of malignant to benign tumours is greatest (>2.3:1) in
the sublingual gland, tongue, floor of the mouth and retro-molar area4. The likelihood,
then of a salivary gland tumours being malignant is more or less inversely
proportional to the size of the gland5, 6
.
2
These tumours usually occur in adults with a female predominance, but about
5% occur in children less than 16years7. WT are more common in males
5, 6. Benign
tumours most often occur in younger individuals, the malignant ones tend to appear in
older age group.
The incidence of parotid tumours is in-between 1-3 / 1lakh/ year,
approximately 75-85% of the salivary gland neoplasm occur in parotid of which 70 -
80% is benign and 80% of the benign tumours are pleomorphic adenoma8. 80 % of
parotid tumours are located in the superficial lobe. Deep lobe neoplasms are
considered to have a greater incidence of malignancy. They exhibit a wide variety of
behaviour and widely diversified histology. In this part of the world, the problem of
these tumours is more troublesome in management because of their late presentation
due to poor economic condition and lack of awareness of health among the general
population. It is important to note that diffuse swellings usually signify disease of
inflammatory nature. Discrete swelling within the gland usually indicates neoplasia
and rarely replace entire gland until very late. Submandibular gland tumours are twice
as likely to be malignant, compared to parotid. Sublingual gland tumours are unusual,
80% are malignant.
FNAC of salivary gland tumours is advantageous to both the patient and the
clinician because of its immediate results, accuracy, lack of complications and
economy9. Appropriate therapeutic management may be planned earlier, whether it is
local excision for a benign neoplasm, radical surgery for a malignant one or any other
alternate treatment. With non-neoplastic lesions, metastasis and lymph proliferative
disorders, conservative management, chemotherapy or radiotherapy might be
respectively preferable9.
3
In general, disregarding specific histological types, Prognosis is most
favourable in those located in palate, less favourable in parotid and least favourable in
submandibular gland.
The behaviour of these tumours is best described by Ackerman and Deal
Regato, “The usual tumour of the salivary gland is tumour in which the benign variant
is less benign than the usual benign tumour and the malignant variant is less
malignant than the usual malignant tumour.”
In this dissertation an attempt has been made to present various conditions of
the salivary gland swellings admitted in Chigateri General Hospital and Bapuji
Hospital from June 2009 to may 2011. All the cases are analysed and compared to
the data available in literature.
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OBJECTIVES OF THE STUDY
1) To study the age and sex distribution among patients presenting with salivary
gland swellings.
2) To study the mode of clinical presentation of various salivary gland swellings.
3) To study the accuracy of FNAC in the diagnosis of salivary gland swellings
4) To study the methods of current surgical treatment of salivary glands swellings.
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REVIEW OF LITERATURE
HISTORICAL ASPECT
• History of salivary gland disease date backs to times of Hippocrates.
• Although parotid gland has been surgically approached on selective basis for at
least the last 300years, an understanding of parotid anatomy, especially in relation
to the facial nerve, was not made clear until early part of 20 century. Earliest
reports of parotid extirpative surgery were recorded in Dutch literature of late
160010.
• Riolan (1648): First to recognize the glandular substance of parotid glands.
• Lorenzo-Heister (1765): Described the earliest parotidectomy performed but no
importance was given to facial nerve or vascular network within gland.
• Early reports of successful parotidectomies include a publication by Siebold in
1781, as well as reports by McClellan in 1824 and Lisfranc in 1826.
• Heyfelder (1825) was able to avoid facial paralysis while performing
parotidectomy.
• According to Foote and Frazel, term mixed tumour dates from Minssen’s review
in 1874- Which is cited by Ahlbom. This neoplasm was originally designated the
benign mixed tumour in 1866. A name change to pleomorphic adenoma was
suggested in 194811.
• Use of RT for treatment of parotid mixed tumour was suggested by Kirmission in
1904.
• Papillary cystadenoma lymphomatosum was described by Hildebrad in 1895.
One case in English literature was reported by Nicholson in 1923 and in US, was
reported by Warthin in 192912.
6
• In 1926, Schutz reported a case of basal cell adenoma. Kleinasser and Klein
were the first to suggest using the term basal adenoma12.
• The oncocyte, which is derived from Greek word ‘onkoushthai’ meaning swollen
or enlarged, was initially described in 1897 by Schaffer. The one case report of
oncocytoma was by McFarland in 1927. In 1931, Hamper applied the term
oncocyte12.
• Schaffer drew the attention to the high recurrence associated with enucleation13.
• The term mucoepidermoid tumour was one used by Stewart, Foote and Becker in
194512.
• Nasse, in 1892, described 4 parotid adenomas composed of cells that closely
resembled the normal acinar cells. In 1953, Buxton and colleagues were to
describe a malignant potential to many of acinic cell tumours12.
• The preferred terminology for malignant pleomorphic adenoma is the carcinoma
ex pleomorphic adenoma coined in 1970. The single lobe concept was
documented and accepted with the understanding that a ‘surgical’ superficial lobe
could be dissected away from the ‘surgical’ deep lobe maintaining the continuity
and integrity of facial nerve during the dissection. (Furstenberg, McWhorter,
Beahrs, Kidd H.A.)14.
• First Facial nerve preserving parotidectomy was performed by Carwardine in
1907 (Rankow R.M. 1976)10.Superficial parotidectomy with conservation of
facial nerve was suggested by Taylor and Garcelon in 1948.
• Patey (1940) recognized that frequent recurrence after enucleation was the result
of capsular defect15.
• Bailey (1941): stressed importance of capsule and anatomy of VII cranial nerve in
parotid gland16.
7
• In 1942, Kaplan recommended a moderate dose of RT (by today’s standard) for
treatment of parotid malignancy.
• In 1942 Ledeman suggested the routine use of post op RT.
• In 1943 R.M.James developed a more currently popular approach of identifying
the facial nerve trunk as it exits from the stylomastoid foramen17.
• Nerve grafts using great auricular nerve reported in 1945 by Furstenberg, but it
was 15 years before next major series reported by Beahrs18.
• Patey (1954) fully defined and described conservative radical parotidectomy19.
• Karolinske (1960) popularized the use of FNAC in parotid tumours in Karolinska
Institute of Stockholm. Cohen ET alin 1990 achieved an overall Accuracy of
88% for FNAC of salivary gland tumours20.
• Richard L. Fabian in 1994 reported salivary neoplasm are encountered at all
ages. But majority of benign tumours occurs in 3rd and 4
th decades of life and
malignant tumour occur in 5th and 6
th decades of life, 2% occur in children less
than 10years of ages and16% occur in those less than 30yrs of age21.
• Gorden T. Deans.et al in 1995 studied and reported that superficial
parotidectomy is advised for most benign lesions confined to superficial lobe,
although enucleation may be considered in selected cases with small mobile
lesion22.
• McGraw M. and K.Husan in 1997 studied that FNAC can distinguish benign
from malignant parotid disease in 93%. Management of discrete, apparently
benign, parotid lump, whether adenoma or carcinoma, is essentially same. As the
FNAC does not alter the treatment of a discrete parotid lump, no consensus is
currently possible regarding its most appropriate use. Perhaps its value is as a
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screening procedure and to provide a little more information when advising the
patient23.
• Joseph Califano, et al in 1999 reported that approximately 80% salivary gland
tumours are found in parotid, 10-15%in submandibular gland and 5-10%in
Sublingual gland and minor salivary gland. Approximately 80% of parotid
neoplasm are benign and the majority if sublingual and minor salivary gland
tumours are malignant24.
• Multiple separate tumours developing in a single salivary gland though rare in
previously untreated person’s two cases of multicentre pleomorphic adenoma in
patients with no previous history of surgery or trauma has been reported25.
• An unusual case of recurrent salivary swelling as a result of sialolithiasis of an
accessory parotid gland, which lay isolated from the main parotid gland, was
reported. The calculi had developed in the accessory salivary tissue with their
absence on in the major salivary glands26.
• Lipoma of the deep parotid gland though a rare clinical entity, about 10 cases has
been reported till now, hence should be considered in the differential diagnosis27.
• A two year study of clinic-pathology of primary salivary gland tumours conducted
at SMHS hospital in Kashmir from AUG-1998 to AUG-2000 revealed, median
age of benign tumours is 4th decade; malignant tumours are in 5
th decade. Out of
100 cases parotid was involved in 70percent of the cases with pleomorphic
adenoma forming the largest group of tumour sites, FNAC diagnosis correlated
with histopathological diagnosis in 98.4 percent of cases28.
• A 12 year study by a Turkish literature, conducted by department of pathology
and otorhinolaryngology, CUKUROVA University concerning FNAC, revealed
9
that FNAC has 94% sensitivity and 100%specificity in diagnosing salivary gland
conditions29.
• The major salivary gland lesions lend themselves well to ultrasound examination
owing to their location and their soft tissue characteristics and are the initial
imaging modality of choice for investigating focal salivary gland lesions and with
good interpretation it obviates the need for CT/MRI30.
• In the Journal laryngoscope 2010 may, submandibular gland excision was
traditionally performed by trans-cervical approach .In order to avoid or reduce
visible scarring and nerve injury , Endoscopic submandibular gland excision via
a hairline incision is now feasible and has resulted in an excellent surgical and
cosmetic outcome31.
10
ANATOMY
Definition:
Salivary gland is any cell or organ which discharges a secretion into the oral
cavity.
Major salivary glands:
They lie at some distance from oral mucosa, with which they communicate
through one or more extra glandular duct. Comprise 3 pairs namely
- Parotid gland
- Submandibular gland
- Sublingual gland
The Parotid gland is the largest (14 to 28gm). The submandibular gland is
about 1/4th the Size of parotid (7-8gm) and the sublingual gland is about 1/3rd the
size (3g) of Submandibular gland.
Minor salivary glands:
They lie in mucosa or sub mucosa and open directly or indirectly via many
short excretory (collecting) ducts, on to the epithelial surface of the mucosa. They
comprises anterior lingual gland, mucus membrane of tongue, small labial, buccal and
palatal gland in relation to mucus membrane of the lips, cheek and roof of mouth
respectively.
Ectopic salivary glands:
Present in any of the following sites i.e. eyelid, lacrimal gland, middle ear,
PNS, nose, jaws, skin of the face and neck32.
11
Figure 1: Anatomy Of Salivary Glands
12
EMBRYOLOGY
Salivary glands are derived from ectoderm layer of the oral cavity. There are 3
stages of development of salivary glands.
1. Branching dichotomous ducts (solid epithelial bud) develop from the salivary
anlagen.
2. Duct acquires lumen and gland lobular form and continues through 7th embryonic
month.
3. Begins in 5th embryonic month, with differentiation of acini and further
maturation of gland, surrounding mesenchyma forms the capsule and interlobular
septet for the parotid gland and submandibular gland. Early in development of the
salivary glands, the primitive duct buds are composed of inner lining of duct cells
and an outer myoepithelial cell layer. At later stage of development, as the
branching duct system acquires spherical glandular acini, the number of the
myoepithelial cells decreases, until they eventually are located only at the distal
segments of ducts and in the primitive acini33.
• Parotid gland developed, beginning in 6 week of intrauterine life. An elongated
furrow running dorsally from the angle of mouth between the mandibular arch and
maxillary process is formed. Groove is converted into a tube, loses its connection
with epithelium of mouth, except at its ventral end, and grooves dorsally into the
substance of cheek. The tube persists as a parotid duct and its blind end
proliferates to form the gland. The interstitium in which parotid gland develop is
rich in lymphoid tissue; this explains why intra-glandular lymph nodes are
relatively abundant and why epithelial glandular tissue inclusion are frequently
seen within some of parotid lymph nodes. This feature is almost totally absent in
Submandibular and Sublingual glands. Sebaceous glands are rarely found in the
13
parotid gland. The acinar cells occur from pre-existing acini and other cells of
ductal origin. The origin of myoepithelial cells is not known. As the gland
arborises posterior, the facial nerve migrates anteriorly through it. Since parotid
ductal branching and facial nerve migration occurs before the condensation of the
mesenchyme, gland and nerve develop an intimate relationship32.
• Submandibular gland begins to develop in the 6 week of IUL. Unlike parotid, it
develops as a relatively discrete structure with early condensation of its
mesenchyma it develops as an epithelial outgrowth from the floor of the linguo-
gingival groove.
• Sublingual gland begins to develop in 8 week of IUL as a number of small
epithelial thickenings in the linguo-gingival groove32.
Figure 2: The origin of parotid submandibular gland and
sublingual gland from the epithelial lining of the primitive
stomodeum is illustrated in the schematic drawing of the
oral cavity of a 9-week-old embryo
14
HISTOLOGY
Both major and minor Salivary glands possess acinar and duct system. These
glands may be of the serous, the mucous, or the mixed, sero-mucous type. The parotid
and the vonebner’s glands of the tongue are exclusively of serous make up. The
palatal Salivary gland and those situated at the base and lateral border of the tongue
are predominantly of the mucous type. The submandibular gland is mixed as it has
both serous and mucous components, but predominantly serous; while Sublingual
gland is also mixed but predominantly mucous.
Saliva is formed by the acinar cells which contain well-developed
endoplasmic reticulum and Golgi bodies with abundant secretary granules and
unmyelinated nerve terminals with numerous synaptic vesicles just between the acinar
cells indicating autonomic innervations. Large basally located intercellular capillaries
characterize these acinar cells.
The mucous acinar cells are arranged around an empty lumen and have a well
rounded basally located nucleus.
The myoepithelial cells (Zimmerman’s cells), also referred to as basket cells,
as they ensheath the individual acini. The encasement forms the basis of the acini.
These are located around the periphery of the acini and intercalated duct. They appear
to have the ability to contact and expel saliva from the acini. The myoepithelial cells
also seem to play an important role in the transport and basement membrane function.
15
Figure 4: Diagram of secretary units at the end of a small duct of salivary
gland. Mucous and serous units are the things to notice here plus a serous
demilune capping themucous tubule at the right (“Demilune” means “half
moon”) compare the position of the nuclei within serous V/s mucous cells
Figure 3: The morphology of the major salivary glands is characterized by
three types of secretary unit. In the parotid (A ) the intercalated duct ( I ) is
longer than in the submaxillary ( B ) and sublingual glands ( C ). In
contrast, the striated duct ( S ) is longer in the submaxillary gland
16
HISTOLOGY OF THE DUCTAL SYSTEM
The cells of the striated ducts are well differentiated and show features
common to the renal proximal tubule cells. These cells play an important role in water
and electrolyte transportation. The intricate duct system is composed of 3 distinct
elements, namely, the intercalated, the striated, and the interlobular ducts. The
intercalated duct is quite short and is lined by a single layer of cuboidal epithelial cells
backed by myoepithelial cells on the outside. The striated ducts are lined by columnar
epithelial cells featuring a luminal brush border. The most important function of these
ducts is active saliva secretion. The terminal portion of the duct system is formed by
intercalated ducts. Depending on the circumference of these ducts, multiple striated
layers of epithelial cells are present. Elastic and collagen fibres surround the
periphery, facilitating the active transport of saliva through the system34.
The intercalated ducts and acini represent the terminal position of the system
(duct acinar unit) under normal conditions; the reserve cells of the intercalated ducts
are the source of regeneration of the acinar tissue and the terminal duct system and are
thought to be the progenitors of most salivary gland tumours. However it has been
pointed out that the basal and luminal cells at all levels of the duct system and even
acinar cells are capable of DNA synthesis and mitosis and therefore they all have the
potential to give rise to neoplasm34.
The lymphoid tissue of the region is represented by small nodes located near
or within the parotid gland and by scattered lymphoid cells located in the connective
tissue around the acini and ducts. The latter are thought to be a part of the MALT.
17
SURGICAL ANATOMY
PAROTID GLAND:
(Para-otic means by the side of ear)It is the largest and has an average weight
of 25gms. It forms an irregular, lobulated, yellowish mass, lying below the external
acoustic meatus and is wedged between mandible and the mastoid; it projects forward
on to the surface of the masseter, where a small part of it, usually more or less
detached, lie between the zygomatic arch above and the parotid duct below; this
detached portion is named as accessory part of gland, present in 20% of individuals.
The parotid gland is like an inverted, flattened 3 sided pyramid, bases of
which is the superior pole and tail/apex- inferior pole; 3 borders, namely, anterior,
posterior and medial; 3 surfaces namely, lateral, antero-medial and postero-medial.
Although not found in every gland, 3 - 5 process of parotid gland exist, making it
Extremely difficult to perform a total parotidectomy.
Three superficial processes:
1) Condylar process near the TM joint,
2) Meatal process in the medial area of the incisura of external auditory canal,
3) Posterior process- projecting between the mastoid and S.C.M. muscle.
Two deep processes:
1) Tympanic process rest on temporal bone
2) Stylomandibular process projects anteromedially above the stylomandibular
ligament.
18
Fascial coverings:
The parotid gland is contained within the investing layer of deep fascia of the
neck, which splits to enclose it.
RELATIONS
Base:
The base is concave and related to posterior surface of TM joint, cartilaginous
part of the external acoustic meatus and tympanic plate from before backwards.
Auriculotemporal nerve and the superficial temporal vessels emerge from its
surface.
Apex:
The apex lies on the posterior belly of digastrics muscle behind angle of the
mandible. The cervical branch of the facial nerve and two divisions of the
retromandibular vein emerge from the apex.
The Lateral Surface:
The lateral surface is related to the superficial fascia, facial branch of greater
auricular nerve, posterior border of platysma and preauricular lymph nodes.
The Anteromedial Surface:
The anteromedial surface has masseter muscle, ramus of mandible and the
medial pterygoid related to it from without inwards. The maxillary artery leaves this
surface and the terminal branches of the facial nerve leaves this, at its anterior border.
19
The Posteromedial Surface:
The poster medial surface is related to sternocleidomastoid muscle, mastoid
process, posterior belly of digastrics and styloid apparatus (styloid process and
structures arising from it) from without inwards. The facial nerve trunk and the
terminal part of external carotid artery (which grooves this surface before entering)
enter this surface.
Structure within parotid substance: These from without inwards are
• Facial nerve and its branches,
• Retromandibular vein and its tributaries (superficial temporal and maxillary veins)
• External carotid artery and its branches (superficial temporal and maxillary
arteries).
• The retromandibular vein joins the posterior auricular vein to form the
external jugular vein.
• Facial nerve has 2 divisions namely tempero-facial and cervico- facial behind
posterior border of ramus of mandible. A plane formed by joining the facial nerve
and the retromandibular vein is called the facio- venous plane of patey. This
plane divides the parotid into a superficial lobe (constitute 4/5 of the gland bulk)
and deep lobe. There is a waist like constriction of the gland that lies between the
ramus of mandible and posterior belly of the digastrics muscle known as isthmus.
Parotid duct:
It arises from the deep surface of the gland on its anterior aspect and unites
with the duct from the superficial lobe and accessory gland at the anterior border of
the masseter muscle. It runs an inch below the zygoma and is 5cm long. At anterior
20
border of masseter, it runs inwards to pierce successively the corpus adiposum
(suctorial pad of infants, bucco pharyngeal fascia and the buccinators to open upon a
small papilla in the vestibule of the mouth opposite the crown of upper second molar
tooth. The lower buccal branch of facial nerve is below the duct and upper branch is
above the duct. Duct wall is thick, with an external fibrous layer containing non-
striated muscle and mucosa is lined by columnar epithelium. Its calibre is 3mm but
smaller at its oral orifice32.
Surface marking:
The parotid gland is marked by lines connecting the following points
successfully.
1) A point on the mastoid tip.
2) A point on the condoyle of the mandible.
3) A point on the middle of the masseter muscle.
4) A point below and behind angle of the mandible.
The parotid duct
Is marked by the mid third of a line joining the philtrum of the upper lip to the
tragus of the ear.
Histology: It shows 3 characteristics.
1) Serous acini and few mucous acini
2) Plenty of ducts,
3) Fat in between these two.
21
Blood Supply:
• Arterial supply is from external carotid artery and its 2 terminal branches.
• Venous drainage is to retromandibular and external jugular veins.
• Lymphatic drainage: Parotid nodes (present within the capsule of the gland, both
on the surface and within the parenchyma) and thence to upper deep cervical
nodes.
Nerve Supply:
Parasympathetic nerve fibres are secreto-motor in nature and arrive to the
gland through the auriculotemporal nerve from the inferior salivary nucleus, present at
the medulla. The tympanic branches from the facial and the glassopharyngeal nerve
form a tympanic plexus in the petrous temporal bone, from which lesser petrosal
nerve arises and contributes fibres to the otic ganglion which is in turn is attached to
the auriculotemporal nerve.
Sympathetic nerve fibres are vasomotor in nature and arise from the plexus on
the external carotid artery with the superior cervical ganglion as the primary source of
supply.
Sensory supply is from the auriculotemporal nerve to the gland and the greater
auricular nerve (C2) to the fascia.
Facial Nerve:
It arises from 2 nuclei in the lower Pons, namely the main motor nucleus and
the smaller nucleus giving rise to the nervus intermedius, which contains
parasympathetic and sensory nerve fibres. The facial nerve enters the internal acoustic
meatus and after variable course in the petrous temporal bone exits through the
22
stylomastoid foramen. It then enters the parotid gland and divides into its 2 main
divisions, upper tempero facial and lower cervico facial. 1cm of nerve is available
before entry into the gland and another 1cm after entering the gland before nerve
divides. The 2 main divisions, in turn again divide into 5-6 terminal branches. These
form an appearance of a duck’s feet and are called pesanserinus. The terminal
branches are temporal, zygomatic, buccal, from the zygomatico-facial division and
mandibular and cervical from the cervicofacial division.
Applied Anatomy:
1. The parotid gland is considered to be a ‘u’ shaped structure with no separate
lobes, by some. But Patey’s plane divides the gland into 2 lobes arbitrarily, and
forms a convenient level for dissecting out tumours confined to the superficial
part.
2. Malignant tumours of the gland infiltrate and invade the facial nerve, causing
partial or total paresis while benign tumours rarely do so.
3. The preauricular lymph nodes are superficial to the parotid capsule and constant in
location viz., anterior to the tragus. But parotid nodes are deeper to the capsule
and can be found in 3 location viz., on the surface of the gland, within the
parenchyma of the gland and deeper to the gland between it and the lateral wall of
the pharynx. It is important to remove all nodes in total parotidectomy.
23
Figure 5: Anatomical Relations of Parotid Gland
Figure 6: Histology of Parotid Glands
24
SUBMANDIBULAR SALIVARY GLAND
It is the 2nd largest salivary gland, situated in digastrics triangle. It is about size
of walnut, horizontally placed ‘U’ shaped, with the limb of U wrapping posterior free
edge of mylohyoid muscle. Upper limb of U is deep to mylohyoid (deep lobe). Lower
limb is superficial to mylohyoid (superficial lobe), which anteriorly reaches anterior
belly of digastric and backward to stylomandibular ligament which intervenes
between submandibular and parotid gland.
Facial covering:
The investing layer of deep cervical fascia splits to 2 leaves enclose the
superficial lobe. Superficial layer attaches to the inferior margin of the mandible and
deep layer to the mylohyoid line of the mandible.
Relations:
The superficial lobe has 3 surfaces-
1) Inferior surface is related the skin, platysma, deep fascia and crossed by cervical
branch of facial nerve and facial vein
2) Lateral surface is related to the submandibular fosse of the mandible and insertion
of Medial pterygoid.
3) Medial surface is related the mylohyoid anteriorly and to the posterior belly of
digastrics, stylohyoid muscle and ligament, facial artery and glassopharyngeal
nerve posteriorly. The deep lobe lies in the intermuscular interval between
mylohyoid below and lateral, and hyoglossus and styloglossus medially; above it
is related to the lingual nerve and below to the hypoglossal nerve and deep lingual
vein.
25
Submandibular Duct:
It is 5cm long and 3mm wide. It begins as numerous branches in superficial
region and emerging from the middle of deep surface of the gland. It runs through the
deep lobe passing 1 upwards and slightly backwards for 4-5 mm and then turns
forward to run between mylohyoid and the hyoglossus. The lingual nerve lies above
the gland and hooks around the inferior aspect of the duct to pass from lateral to
medial side. It opens into sublingual papilla through an ostium, one on either side of
fraenulum of the tongue.
Blood Supply:
• Arterial supply is from facial artery and a few twigs of the lingual artery.
• Venous drainage is to common facial and lingual veins.
• Lymphatic drainage is to submandibular and upper deep cervical nodes.
Nerve Supply:
• Parasympathetic nerve fibres (secretomotor) come through the lingual nerve and
its chorda tympani branch from the superior salivary nucleus in the lower Pons in
the brain.
• Sympathetic nerve fibres (vasomotor) arrive to the gland from the plexus on the
facial artery, the primary source of supply being the superior cervical ganglion.
Histology: It has serous and mucinous acini in equal in number and few ducts.
26
Applied Aspects:
1. Submandibular gland is related to 2 nerves on superficial aspect (marginal
mandibular and cervical divisions of facial nerve) and 2 nerves on its deeper
aspect (lingual and hypoglossal). These should be protected during surgery.
2. Submandibular gland is palpable bi digitally only when the whole gland is
enlarged. But it is difficult to differentiate swelling of superficial lobe from
submandibular lymph nodes clinically.
3. Because of the proximity of gland to the mandible, malignant tumours of the
gland get fixed to the bone more often than parotid tumours. The mandible along
with the primary growth and enlarged lymph nodes has to be removed Enbloc to
obtain adequate local control of the disease.
4. Submandibular lymph nodes are important drainage zone for head and neck
tumours. During block dissection of lymph nodes the submandibular gland with
its contained nodes is removed.
Figure 7: Anatomy of Sub Mandibular Salivary Glands
27
Figure 8: Histology of Submandibular Salivary Gland
28
SUBLINGUAL GLAND
The Sublingual gland is the smallest of the paired salivary glands. It weighs 3-
4 gm each and is narrow, flattened and almond shaped.
• Relations: It lies under the mucous membrane of the mouth.
• Medially is the genioglossus muscle with the submandibular duct and lingual
nerve intervening in middle.
• Laterally: the sublingual fossa of the mandible above the anterior part of
mylohyoid line.
• Inferiorly: is the mylohyoid muscle.
• Anteriorly: it is related to its fellow of opposite side.
• Posteriorly: related to deep part of submandibular gland.
• Ducts: 8-20 in number and open directly and separately into floor of the mouth on
summit of sublingual fold or indirectly into the submandibular duct. These ducts
are called the ducts of Rivinus.
Blood supply:
• Arterial supply is from facial and lingual arteries.
• Venous drainage is to lingual veins.
• Lymphatic drainage is to submandibular lymph nodes.
Nerve supply:
Parasympathetic fibres are secretomotor and arrive from superior salivary
nucleus. Sympathetic is from same source as submandibular gland.
• Histology: It has purely mucinous acini and plenty of ducts36
29
Figure 9: Anatomy of Sublingual Salivary Glands
Figure 10: Histology of Sublingual Salivary Glands
30
ANATOMY OF MINOR SALIVARY GLANDS
Minor salivary glands (500-1000, 1-5 mm each) are located throughout the
submucosa of the oral cavity.
• The anatomic distribution of minor salivary glands show that hard and soft palate
are the most common anatomic sites, followed by maxillary sinus, upper lip
mucosa, oral mucoosa of the cheek area, gigiva, nasopharynx and pharynx,
tongue, lower lip mucosa and larynx
• More numerous in posterior hard palate
- Each salivary unit has its own simple duct
- Most of these minor salivary glands are mucinous with the main exception of
Ebner’s glands which are serous glands located in the circumvallate papillae
of the tongue
• The minor salivary glands are important components of the oral cavity, present in
most parts of the mouth, and their secretions directly bathe the tissues. Individual
glands are usually in the submucosa between muscle fibres, and consist of groups
of secretory endpieces made up of mucous acinar cells and serous or seromucous
demilune cells112
.
31
PHYSIOLOGY
The total salivary secretion is 1 to 1.5 litres per day with a pH between 7.0 -
8.0.
Functions of Saliva:
1. Moistening dry foods to aid swallowing (lubrication).
2. Providing a medium for dissolved and suspended food materials that chemically
stimulate taste Buds.
3. Buffering of the contents of oral cavity through its high HCO3 ions concentration.
4. Digestion of carbohydrate by the digestive enzymes ±-amylase that breaks the 1-
4 glycosides bonds and continues to act in the oesophagus and stomach.
5. Controlling the bacterial flora of the oral cavity because of the presence of
antibacterial Enzyme lysosyme.
6. As a source of calcium and phosphate ions essential for normal tooth
development and maintenance.
7. Immunologic functions of saliva - IGA.
Control of Salivary Secretion:
Parasympathetic nerve stimulation causes, profuse watery secretion and
sympathetic nerve stimulation causes thick scanty secretions. There are phases of
secretion, namely
• Cephalic phase: In which smell sight and the thought of the food causes
salivation; Oral phase in which when food enters the mouth the salivation is
induced.
32
• Gastric phase: In which food entering the stomach causes salivary secretion.
Salivary gland controlled mainly by PNS from the salivary nuclei. The salivary
nuclei are located at junction of the medulla and Pons and are excited by both
taste and tactile stimuli from the tongue and other areas of the mouth. Many taste
stimuli, especially the sour taste, elicit copious secretion of saliva.
Salivary secretion is also stimulated or inhibited by impulses arriving from the
higher centres of the CNS. The appropriate areas in the brain, which regulates these
effects are located in close proximate to the parasympathetic centres of the anterior
hypothalamus, and it functions to its great extent in response to signal from the taste
and smell areas of the cerebral cortex or amygdala. Salivation also occurs in response
to reflexes originating in the stomach and upper intestine. Sympathetic stimulation
can also increase salivation to a moderate amount, but much less so than the
parasympathetic stimulation.
Salivary Gland Histology Nature Of Secretion Quantity Of
Secretion (%)
Parotid Serous Watery 20
Submandibular Seromucinous Moderately Viscous 70
Sublingual Mucinous Viscous 5
Sympathetic nerves originate from the superior cervical ganglia and then
travel along blood vessel to the salivary gland11, 37
.
33
BIOCHEMISTRY
The specific gravity of saliva varies from 1.002 to 1.012. Viscosities of the 3
major Salivary glands are Parotid-1.5, Submandibular-3.4 and Sublingual-
13.4centipoises. PH is slightly acidic prior to secretion but slightly alkaline upon
entering oral cavity from loss of CO2. About 90% of total volume of saliva comes
from parotid and submandibular glands in approximately equal amounts. Sublingual
glands contribute 3%37.
Composition of Saliva:
Substance Mean Value Parotid Submandibular
Flow rate
(ml/min/gland; stimulated)
Inorganic analytes (meq/l)
0.7
0.6
K+
Na++
Cl-
HCO3-
Ca++
Mg++
HPO42- (mg/dl)
20
23
23
20
2
0.2
6
17
21
20
18
3.6
0.3
4.5
Organic analytes (mg/dl)
Urea 15 7
Protein 250 150
Ammonia 0.3 0.2
Uric acid 3 2
Lysozymes 2.3 105
Glucose <1 <1
IgA 4 2.0
Amylase
Cholesterol
pH
fatty acids
total lipids
amino acids
0.1
<1
5.92
1
2-6
1.5
0.002
-
5.73
-
2-6
-
34
CLASSIFICATION
Salivary gland disorders can be broadly classified as
• Acute Inflammatory Lesions
- Mumps
- Acute Suppurative Sialadenitis
• Chronic Inflammatory Disorders
• Granulomatous Diseases
- Primary Tuberculosis of the Salivary Glands
- Animal Scratch Disease
- Sarcoidosis
- Sjögren's Syndrome
- Sialolithiasis
• Cystic Lesions
• Radiation Injury
• Trauma
• Sialadenosis
• Other Disorders
• Neoplastic Disorders
- Benign
- Malignant
35
WHO CLINICAL CLASSIFICATION OF SALIVARY GLAND TUMOURS
(1991)38
I. Adenomas
1) Pleomorphic adenoma
2) Warthin’s tumour
II. Carcinomas
1) Acinic cell carcinoma
2) Mucoepidermoid carcinoma
3) Adenoid cystic carcinoma
4) Adenicarcinoma
5) Squamous cell carcinoma
6) Undifferentiated carcinoma
7) Carcinoma in pleomorphic adenoma
III. Non-Epithelial Tumours
1) Haemangioma
2) Lymphangioma
3) Neurofibroma
4) Neurilemoma
IV. Malignant Lyphoma
V. Unclassified and Allied Conditions
36
ETIOLOGY OF SALIVARY GLAND SWELLINGS
Salivary gland can be affected by a wide variety of disorders39.
1. Acute Bacterial and Viral Infection of Salivary Glands
Bacterial infection: It plays a most important role in the etio-pathogenesis of salivary
gland swellings. Bacterial infections of the salivary gland swellings results from two
important physiological mechanism.
• Retrograde contamination of the salivary ducts and parenchyma tissues by
bacteria inhabitating the oral cavity
• Stasis of the salivary flow through the ducts and parenchyma.
• Sialolithiasis can produce mechanical obstruction of the duct, resulting in salivary
stasis and subsequent bacterial infection, about 85-90% of salivary calculi are
located in the submandibular duct because
- Submandibular secretions are more mucinous and viscid compared to parotid
secretions.
- They are more alkaline and contain a high percentage of calcium phosphates.
- Despite the submandibular gland’s predisposition for calculus formation, the
parotid gland remains the most common site of acute suppurative salivary
infection.
• Viral infection: A broad range of viral pathogens have been identified as a cause
of acute viral Infections of the salivary glands usually spread by air-borne droplets
in the Community, “mumps” is classically designated as a viral parotitis caused by
Paromyxoma virus.40
37
2. Chronic Sialadenitis
Chronic sialadenitis is believed to be due to lowered secretion rate with
subsequent salivary stasis, like acute sialadenitis it is more common in parotid gland
and usually occurs from permanent damage to the gland from acute suppurative
infection41.
3. Sialolithiasis:
Sialolithiasis is one of the most common causes of salivary gland swellings.
The exact cause of calculi formation is not clear weather chronic sialadenitis
instigates the calculi formation or vice versa. But it is clear that genesis of calculi lies
in relative stagnation of a calcium rich saliva42.
4. Sialadenosis
Sialadenosis is a non specific term used to describe a non-inflammatory, non-
neoplastic enlargement of a salivary gland, usually the parotid. The enlargement is
generally asymptomatic and the mechanism is unknown in many cases. Bilateral
parotid gland swelling is common in obesity43.
5. Mucoceles:
The mucocele, the oral ranula, and the cervical, or plunging, ranula are clinical
terms for a pseudocyst that is associated with mucus extravasation into the
surrounding soft tissues. These lesions occur as the result of trauma or obstruction to
the salivary gland excretory duct and spillage of mucin into the surrounding soft
tissues.
38
Ranulas are mucoceles that occur in the floor of the mouth and usually involve
the major salivary glands. Specifically, the ranula originates in the body of the
sublingual gland, in the ducts of Rivini of the sublingual gland, in the Wharton duct of
the submandibular gland, and, infrequently from the minor salivary glands at this
location.
These lesions are divided into 2 types oral ranulas and cervical or plunging
ranulas.
a) Oral ranulas are secondary to mucus extravasation that pools superior to the
mylohyoid muscle.
b) Cervical ranulas are associated with mucus extravasation along the fascial planes
of the neck.
Pathophysiology of Mucus Retention Cyst
• The development of mucoceles and ranulas depend on the disruption of the flow
of saliva from the secretory apparatus of the salivary glands
• Trauma that results in damage to the glandular parenchymal cells in the salivary
gland lobules is another potential mechanism.
• Most oral ranulas originate from the secretions of the sublingual gland, they may
develop from the secretions of the submandibular gland duct or the minor salivary
glands on the floor of the mouth. The mucus extravasation of the sublingual gland
almost exclusively causes cervical ranulas. The mucus escapes through openings
or dehiscence in the underlying mylohyoid muscle.
6. Salivary Gland Tumours
Many factors have been implicated in the cause of the salivary gland tumours.
39
• Viruses: The Epstein- bar virus and possibly auto-immunity lead to salivary gland
carcinoma referred to as malignant lympho-epithelial lesion. Other viruses may
also be associated with salivary gland neoplasm in mice like polyoma virus, CMV
and human papilloma virus types 16 and 182.
• Radiation:
Substantial evidence exists from a relationship between exposure to ionising
radiation and the later development of salivary gland tumours.
a) Japanese people, who were exposed to radiation generated by the atomic
bombs dropped on Hiroshima and Nagasaki, have demonstrated increased risk
for developments of salivary gland tumours.
b) The tumorogenic effects of therapeutic radiation to the head and neck on
salivary gland tissue have been assessed in Michael Reese hospital in Chicago.
There was a 40 fold increase in risk for the development of malignant tumours
in irradiated population compared to the normal population.
c) There is association between developments of malignant parotid tumours in
patients who had five or more full mouth dental radiographic series before
196044.
• Occupation: Certain occupation has been reported to place the people at
increased risk for the development of salivary gland carcinoma. These include
asbestos mining, manufacturing of rubber products and industries such as shoe
manufacturing, plumbing and wood working in the automobile industries45.
• Hormones: Endogenous hormones may have a role in the carcinogenesis of
salivary gland tumours. Salivary gland tumours in woman have increased
estrogens receptor levels and also prolactin binding activity45
40
• Others: Musebeck (1966), considers that local or general diseases or disturbance
of regulation effect the Salivary glands and contribute to tumour production,
especially adenolymphomas46.
Histogenesis of Salivary Gland Tumours:
Majority of Salivary gland neoplasm arises from immature/ reserved cells
which are Important for tissue renewal. Two theories have been proposed for
histogenesis.
• Multi-cellular theory states that a salivary gland neoplasm arises from the adult
Differentiated counterpart of the salivary gland unit.
• Bicellular theory: It is now generally agreed, as one pointed out in 1971, that the
basal cells of the excretory and intercalated duct acts as reserve cells for the more
differentiated cells of the salivary gland unit. To the light microscopic evidence
can now be added data from electron microscopic studies which further support
the theory that all salivary gland epithelial neoplasm arises from these 2 cells
(excretory duct reserve cell and the intercalated duct reserve cell) and not by
dedifferentiation of their mature counter parts.
Thus neoplasia is the result of disease of the reserve cells, which are
responsible for tissue renewal, and not of the fully differentiated cells. The genome of
these cells contains the information needed to undergo normal development or to
become a benign or malignant neoplasia. Malignant degeneration of normal
differentiated cells does not occur47.
41
Histogenesis of Salivary Gland Neoplasms47
• Multicellular
Oncocytic tumours derived from Striated duct cells
Acinous Tumours derived from Acinar cells
Squamous cell carcinoma derived from Excretory duct cells
Mucoepidermoid
carcinoma
derived from Excretory duct cells
Mixed tumours derived from Intercalated duct cells and
Myoepithelial cells
• Bicellular Theory
Intercalated duct reserve cells • Pleomorphic adenoma
• Warthin’s tumor
• Oncocytoma
• Acinous cell tumors
Excretory duct reserve cells • Squamous cell carcinoma
• Mucoepidermoid carcinoma
42
PATHOLOGY
A salivary gland tumour, by its complex histological appearance, makes
interpretation Difficult. . One of the pre-requisites for comparative studies is
agreement on criteria for classification of tumours and a standardized nomenclature. It
helps in the comparison of Clinico-pathological observation by various workers in the
field.
Classification by Foote and Franzell 1954
Benign Malignant
1. Papillary Cystadenoma
lymphomatosum
1. Malignant mixed tumor
2. Oxyphil adenoma low grade and high
grade
2. Mucoepidermoid tumor, low grade
and high grade
3. Sebaceous cell Adenom 3. Squamous cell Carcinoma
4. Benign Lymphoepithelial lesion 4. Adenocarcinoma
5. Unclassified 5. Adenoid cystic Carcinoma
6. Trabacular or Solid Carcinoma
7. Anaplastic Carcinoma
8. Mucous cell Carcinoma
9. Pseudo adamantine Carcinoma
10. Acinic cell Carcinoma
Although the salivary glands are simple structurally, their ducts and acini give
rise to a variety of histological distinct tumour types, even within one particular
43
lesion and this has caused considerable problem in categorization and diagnosis. This
is illustrated by the plethora of classification systems developed over the years.
Simpson RHW 1994 studied AFIP morphologic classification and the revised
WHO classification and found that later is better in that it is not excessively long; it
allows majority of tumours to be correctly categorized and is readily applicable in
practice.
Revised WHO Histological Classification (Siefort & Sobin 1992)
1. Adenomas
1.1 Pleomorphic adenoma
1.2 Myoepithelioma (Myoepithelial adenoma)
1.3 Basal cell adenoma
1.4 Warthin tumor (adenolymphoma)
1.5 Oncocytoma (oncocytic adenoma)
1.6 Canalicular adenoma
1.7 Sebaceous adenoma
1.8 Ductal papilloma
1.8.1 Inverted ductal papilloma
1.8.2 Intraductal papilloma
1.8.3 Sialadenoma papilliferum
1.9 cystadenoma
1.9.1 Papillary cystadenoma
1.9.2 Mucinous cystadenoma
2. Carcinomas
2.1 Acinic cell carcinoma
44
2.2 Mucoepidermoid carcinoma
2.3 Adenoid cystic carcinoma
2.4 Polymorphous low grade adenocarcinoma
2.5 Epithelial- myoepithelial carcinoma
2.6 Basal cell carcinoma
2.7 Sebaceous carcinoma
2.8 Papillary cystadenocarcinoma
2.9 Mucinous adenocarcinoma
2.10 Oncocytic carcinoma
2.11 Salivary duct carcinoma
2.12 Adenocarcinoma (not otherwise specified)
2.13 malignant myoepithelioma (myoepithelial carcinoma)
2.14 carcinoma in pleomorphic adenoma
2.15 squamous cell carcinoma
2.16 small cell carcinoma
2.17 undifferentiated carcinoma
2.18 other carcinoma
3. Nonepithelial tumors
4. Malignant lymphomas
5. Secondary tumors
6. Unclassified tumors
7. Tumor like condition
7.1 Sialadenosis
7.2 Oncocytosis
7.3 Necrotizing sialometaplasia (salivary gland infarction)
45
7.4 benign lymphoepithelial lesions
7.5 salivary gland cyst
7.6 chronic sclerosing sialadenitis of submandibular gland (kuttner tumor)
7.7 Cystic lymphoid hyperplasia in AIDS.
1) Pleomorphic adenoma:
Morphology:
The tumour is typically well circumscribed, thinly encapsulated and solitary,
smooth or lobulated. C/S shows greyish white areas rubbery, fleshy, mucoid or
glistening, depending on the content and amount of the stroma, with translucent bluish
areas which represent cartilage with a myxoid stroma may have slimy consistency11.
Microscopy:
Growth Pattern:
It shows pseudo encapsulation, which is a compressed fibrosed surrounding
salivary gland tissue, into which it sends extensions or pseudopodia, called satillosis
(outgrowth of main mass which can be demonstrated on serial section, they should not
be regarded as evidence of invasion). Hence, simple enucleation is associated with
high rate of recurrence. For this reason, mixed tumour was thought to be a low grade
malignancy, earlier. Occasionally tumour islands may appear outside the capsule.
Basic cellular organization:
Varied histological appearance in different tumours and in different parts of
the same tumours. There is an epithelial component and a stromal component, and
both can be remarkably pleomorphic. The epithelial component consists of epithelial
46
and myoepithelial cells. The prototypic histological appearance consists of narrow
tubular structures enclosed by myoepithelial mantles submerging in a chondromyxoid
stroma. Epithelial component: These may be arranged in anastomosing tubules, small
cysts, ribbons and solid sheets. The cells may be columnar, cuboidal or flat.
Occasionally these cells can undergo metaplastic changes to mucous, goblet or
squamous cells. Myoepithelial Component: These cells appear as cuboidal, spindle,
stellate, plasmacytoid, epitheloid and hydropic clear cells. Since their occurrence is
restricted to PA and Myoepithelioma, their identification is of great diagnostic value.
Stroma:
Extracellular stroma is one of the defining components of PA. The stroma
takes the form of a mixture of chondroid (hyaline cartilage), myxoid, chondromyxoid,
hyaline and rarely osseous and adipose tissues. Tyrosine and oxalate crystals can
develop between the cellular or stromal components and appears to be unique to PA11.
47
PLEOMORHIC ADENOMA
Figure 11: Gross Specimen of Pleomorphic Adenoma
Figure 12: Histopathology of Pleomorphic Adenoma
48
2) Warthin’s tumour (Adenolymphoma/Papillary cystadenoma
lymphomatosum):
Morphology: The tumour is well encapsulated with thin tough capsule which is
usually intact, fluctuant to firm rubbery in consistency. C/S is solid or papillary
reddish grey and shows multiple cysts few mm to cm which is nearly path gnomonic,
its fluid is serous/ mucoid/ chocolate or semisolid caseous material.
Microscopy: Irregular cystic structures in which the lining epithelium is thrown into
papillary folds. The epithelium consists of 2 layers- a luminal layer of oncocytic
columnar cells with darkly stained, pyknotic nucleus centrally placed near the luminal
surface, supported by a discontinuous layer of basal cells (cuboidal/ polygonal cells
with prominent nucleoli). Cytoplasm of both layers is finely granular and distinctly
eosinophilic due to accumulation of mitochondria. The lumen of the cysts contains
thick proteinaceous secretions, cellular debris, cholesterol crystals and sometimes
laminated bodies that resemble corpora amylacea. A distinct layer of basement
membrane separates the papillae or cystic lining from the lymphoid stroma. The
lymphoid stroma consists of small lymphocytes, plasma cells, histiocytes, germinal
centre and sinusoids. The tumour is thought to originate from the heterotypic salivary
tissue, entrapped within the lymph in the vicinity. It is impossible to differentiate the
benign from malignant oncocytoma on gross examination, but the malignant ones are
usually solid12. Combination of lymphoid matrix and papillation of eosinophilic
epithelial cells forming cystic spaces presents a distinct and pathognomonic
histological feature.
The relative proportions of epithelial and lymphoid components in WT vary. 4
subtypes are recognized by Siefert:
49
• Subtype 1(classic WT) is 50% epithelial,
• Subtype 2(stroma poor) is 70-80% epithelial,
• Subtype 3(stroma rich) is only 20-30% epithelial and
• Subtype 4 is characterized by extensive squamous metaplasia51.
Figure 13: Gross Specimen of Warthin’s Tumour
Figure 14: Histopathology of Warthin’s Tumour
50
3) Monomorphic adenoma:
Characteristic feature is monomorphic cellular composition, probable origin
from the intercalated duct reserve cell. They manifest as purely epithelial or purely
mesenchymal growth pattern. In many monomorphic adenomas there are histological
features that recall stages in the embryology of dermal adenexa, as well as salivary
gland.
a) Basal cell adenoma: It is the most common monomorphic adenoma and likely
represents the isocellular counterpart of PA.
Morphology: Well encapsulated, well circumscribed. C/S is uniform and varies from
light tan to brown, homogenous. Surface is usually multifaceted and multinodular.
Microscopy: Small basaloid cells possessing round, uniform, basophilic nuclei and
scant cytoplasm. Nuclear pleomorphism and mitosis are not seen. There are 4
morphological patterns-
1. Solid type: most common pattern. Basaloid cells form broad bands, smooth
contoured islands and solid masses with peripheral palisading which can be so
prominent as to mimic Ameloblastoma. These basaloid cells are sharply
demarcated from highly vascularised stroma by basement membrane.
2. Tubular Type: Least common type, in which discrete or anastomosing tubules
predominate. The tubules are lined by two distinct layers of cells, with inner
cuboidal ductal cells surrounded by an outer layer of basaloid cells.
3. Trabacular Type: This type consists of narrow and broad trabeculae of cells
interconnected with one another, producing a reticular pattern.
51
4. Membranous Type: This differs from other subtypes by the presence of
abundant, thick, eosinophilic and PAS +, hyaline basal lamina material around the
smooth contoured tumour islands.
b) Myoepithelioma:
Morphology: Well circumscribed, frequently well encapsulated that shows no feature
distinct from mixed tumour except for absence of grossly myxoid areas and chondroid
areas.
Microscopy: This type of adenoma consists entirely of myoepithelial cells. The
different type described are, the spindle and stellate myoepithelioma, clear cell variant
and a malignant variety (crissmann J.D. 1977, & Saskela E. 1972).tumours have
scanty intervening hyalinised stroma.
Three morphological patterns
1) Spindle cell- most common especially in parotid. Spindle shaped cells with
eosinophilic cytoplasm arranged in diffuse sheets or interlacing fascicles.
2) Plasmocytoid- commonly seen in palatal tumours.
3) Epitheloid/clear cell- Stroma is scanty, fibrous or myxoid and it occasionally
contains chondroid material52.
c) Oncocytoma (oxyphil adenoma):
Morphology: Well circumscribed and thinly encapsulated. External surface of the
tumour is smooth. The C/S is mahogany brown, solid with focal areas of red brown
haemorrhage.
52
Microscopy: Hallmark of this is presence of oncocyte, polygonal cells possessing
abundant eosinophilic granular cytoplasm as it contains large number of
mitochondria, central round nuclei and often-distinct nucleoli, arranged in solid sheets
or in nests and cords, which form alveolar or organoid patterns, which are separated
by thin fibrous septa or scanty loose vascularised stroma53, 54
.
d) Canalicular Adenoma:
Canalicular adenoma is an uncommon benign salivary gland tumour
exclusively occurring in the intra oral glands. The average age for canalicular
adenoma is 65 years, with a range of 34 to 88 years. The female to male ration is 1.7
to 1. Most common site of occurrence of this tumour is the upper lip and buccal
mucosa.
Gross: The gross appearance of canalicular adenoma varies from a discrete
encapsulated nodule to lesions that are circumscribed, but unencapsulated. The size is
about 1.7 cm in diameter. The colour has been reported to range from pink to tan or
brown or yellow. Cut surface shows cystic spaces with gelatinous mucoid material.
Microscopy: The microscopic appearance of canalicular adenoma is characteristic.
The cells are uniformly cuboidal or columnar. They usually have scanty eosinophilic
cytoplasm with indistinct borders and the nuclear chromatin is diffuse and granular.
The cells are arranged in cords of single cells that form parallel columns producing
long “canals”. Typically, the rows are separated periodically producing ductal
structures. The stroma of canalicular adenoma is delicate, richly vascularised and
sparsely cellular.64
53
Figure 16: Histopathology of Myoepithelioma
Figure 15: Histopathology of Basal Cell Adenoma
TRABECULAR TYPE SOLID TYPE
54
Figure 17: Histopathology of Oncocytoma
Figure 18: Histopathology of Canalicular Adenoma
55
5. Sabaceous Adenoma:
It is a rare tumour and accounts for 0.1% of all salivary gland neoplasm. The
mean age is 58 years, with a range of 22 to 90 years. There is a male preponderance
and parotid glands are commonly involved. This is the only type of sebaceous
neoplasm included in the WHO classification.
Gross: it is encapsulated or sharply circumscribed and varies incolour from gray
white to pinkish white to yellow to yellowish gray.
Microscopy: These tumours are composed of sebaceous cell nests with minimal
atypia and pleomorphism and no tendency to invade local structures. Many tumours
are micro cystic or may be composed predominantly of ectatatic salivary ducts with
focal sebaceous differentiation. Sebaceous glands are usually embedded in fibrous
stroma. Occasionally, oncocytic metaplasia, histocytic infiltration and foreign body
giant cells may be seen focally.65
6. Ductal Papilloma:
Seifert and colleagues apparently included sialadenoma papiliferum,
intraductal papilloma and inverted ductal papilloma with a broad category of
monomorphic adenoma that they called ductal papilloma or adenoma
I. Intraductal Papilloma:
Intraductal papillomas of salivary glands are rare tumours. Age ranges from 29
to 77 years with a mean age of 54 years. Male to female ratio is equal. Minor salivary
glands are the most common site.
Gross: The tumour is usually a well circumscribed cyst with a lumen that is partially
or completely filled with a friable tissue extending from the wall of the cyst.
56
Microscopy: The papilloma appears to arise in the duct system more distant from the
mucosal surface than from where the inverted ductal papilloma arises. This is
unicystic and is composed of papillary fronds that extend into the cystic lumen. The
projections have delicate fibro vascular cores and are covered by cuboidal or
columnar ductal epithelium, similar to that lining the cystically dilated salivary duct.
Mucous cells may be interspersed among the ductal cells.
II. Sialadenoma Papilliferum:
Sialadenoma papilliferum constitutes 0.1% of epithelial salivary gland
tumours and 0.6% of benign epithelial tumours of minor salivary glands. Most of the
cases are older than 50 years and the average age is 56 years. Male to female ratio is
1.5 to 1. Most common site is minor salivary glands.
Gross: It is a round or oval, well circumscribed lesion. The lesions may be broad
based or pedunculated. The surface of the tumour appears rough, pebbly, verrucous or
overtly papillary. The lesion is often reddish. Cut sections reveal cauliflower like
surfaces and circumscribed nodules of the tumour tissue that extend below the level of
the mucosa.
Microscopy: The tumour has exophytic and endophytic components. The outer
portion is a typical papilloma with finger like projections supported by delicate
fibrous connective tissue cores that extend above the level of adjacent mucosa. The
covering epithelium of the fronds is stratified squamous and it can be hyperkeratotic
and parakeratotic.
57
III. Inverted Ductal Papilloma:
It is a rare tumour and occurs in adults ranging in age from 32 to 66 years,
mean age being 50 years. There is no sex predilection. Minor salivary glands are the
most common site.(lower lip and buccal mucosa most frequent)
Gross: Inverted ductal papilloma occurs within the terminal portion of minor salivary
gland excretory duct and therefore resembles a sialadenoma palliferum.
Microscopy: The microscopic features are different from sialadenoma papilleferum. It
produces a bulging growth but it does not extend above the surface mucosa like the
papillary fronds of sialadenoma papilliferum. Well circumscribed mass of basaloid
and squamous cells are arranged in papillary configuration into luminal cavity. They
appear to fill the cavity and extend outwardly into the surrounding lamina propria of
the oral mucosa. The ductal lumen from which the inverted papilloma arises may
communicate with the surface through an opening. It is covered by cuboidal duct cells
and occasionally scattered mucosal cells.66, 67
.
7. Cystadenoma:
These tumours constitute 2.2% of all benign epithelial tumours. These are
most common after the 8th decade of life. There is no difference in the male and
female distribution. Major salivary glands are involved in 65% of the cases and minor
glands in 35% of the cases.
Gross: cystadenoma of the major salivary glands is usually asymptomatic, slowly
enlarging swelling. The minor salivary gland tumours produce smooth nodule that
58
may be compressible. In the series reported by Waldron and co-workers, lesions
measured less than 1cm in diameter. Often the swelling represents a mucocele.
Microscopy: Diagnostic histology criteria of cystadenoma are debated. The tumour is
multicystic, well defined and may be encapsulated. The epithelial lining of the cysts
can be cuboidal, flat or columnar. Oncocytic, as well as mucous changes of the lining
may exist and occasionally are dominant.65
MALIGNANT NEOPLASM
1) Acinic cell carcinoma
Morphology: It is often circumscribed with an incomplete capsule. The C/S is solid,
with or without cystic areas. It is the most common parotid tumour to present as a
cystic mass. The cyst may comprise only a small portion of the tumour or may be
large with only small solid or papillary foci.
Microscopy: They typically form a solitary mass or multiple nodules and invade in
broad fronts. There can be variably prominent lymphoid aggregates, with or without
lymphoid follicle formation. The neoplastic elements recapitulate the appearance of
the acinar-intercalated duct unit. The nuclei are bland looking and mitotic figures are
rare. Cells are arranged most commonly in organoid sheets traversed by ramifying
delicate blood vessels. The lobular architecture is lacking. 3 histological patterns are
recognized.
a) Microcystic pattern: This is the most common pattern with multiple small empty
spaces (micro cysts) producing lacy appearance. The neoplastic acinar cells
possess basophilic granular cytoplasm and basally located nuclei.
59
b) Papillary cystic variant: This is characterized by large cystic spaces lined by
cuboidal epithelium with papillary projections. Hobnail cells, intercalated duct
like cells, vacuolated cells and non-specific glandular cells cover the papillae.
c) Follicular variant: It is less frequent, comprises multiple, closely packed, round
cystic spaces filled with homogenous eosinophilic colloid like material, highly
reminiscent of thyroid follicles55.
60
Solid and microcystic patterns
• Most common
• Solid sheets
• Numerous small cysts
– Polyhedral cells
– Small, dark, eccentric nuclei
– Basophilic granular cytoplasm
Figure 19: Gross Specimen of Acinic Cell Carcinoma
Figure 20: Histopathology of Acinic Cell Carcinoma
61
2) Adenoid Cystic Carcinoma (Cylindromatous carcinoma)
Morphology: C/S shows tan, fleshy, firm invasive tumour.
Microscopy: Infiltrative growth is usually obvious and perineural invasion is very
common. There is no melting of basaloid cells in the stroma. The stroma is fibrous
with variable amounts of myxo-hyaline material. 3 histological patterns are
recognized
a. Cribriform pattern: This is the most characteristic feature giving rise to a sieve
like “Swiss Cheese” pattern. They are variable sized, smooth contoured, discrete
to coalescent islands, comprising small, uniform basaloid cells punctuated by
round sized spaces. Nuclear pleomorphism is usually mild and mitotic figures are
usually few or absent.
b. Tubular pattern: A single layer of ductal epithelial cells with a single or multiple
layers of basaloid cells line the elongated tubules.
c. Solid pattern: Smooth contoured or focally jagged sheets of closely packed
basaloid cells characterize this type. These cells exhibit more significant nuclear
pleomorphism and mitotic figures. The solid growth pattern is rarely present and
if so, may not be recognizable as ADCC56.
62
Histology --
• Cribriform pattern
• MOST common
• “Swiss cheese” appearance
Figure 21: Histopathology of Adenoid Cystic Carcinoma
63
• Mucus cell > epidermoid cells
• Prominent cysts
• Mature cellular elements
Figure 22: Histopathology of Mucoepidermoid Carcinoma
64
3) Mucoepidermoid Carcinoma
Gross: They have ill-defined mass, which may be partially encapsulated.
Microscopy: It comprises haphazardly dispersed mucin filled cysts, irregular tumour
nests composed of mucous, squamous (epidermoid) and nondescript intermediate
cells. Although the tumour borders can be circumscribed, most cases exhibit irregular
invasive border at least focally.
� Low grade MEC: Mucin filled cystic structures constitute large proportions of
the tumour and there are abundant mucous cells. Cells have bland nuclei and
mitosis rarely seen. The intracellular mucin can be demonstrated readily by
mucicarmine or diastase-PAS stain. Another major cell type is the intermediate
cell which is polygonal and has a non-descript appearance. Squamoid cells occur
in nests or line cystic spaces. The lymphoid component may be exuberant in the
stroma.
� High grade MEC: Contains more solid areas and few cystic spaces, perineural
and intravascular invasion are common. The solid areas are formed by large
polygonal squamoid cells with pale to eosinophilic cytoplasm and distinct cell
borders, as well as intermediate cells. Squamoid features are often better
developed compared with low-grade tumours. Cellular pleomorphism, nuclear
hyperchromasia and mitosis are more impressive and areas of coagulative necrosis
may be present.
� Intermediate Grade: The intermediate grade tumour is histological between low
and high-grade tumours. Some degrees of nuclear pleomorphism are observed in
the tumour cells. Cystic spaces do not constitute a significant portion of the
tumour.
65
Variants: Pan Sclerosing variant shows keloid like sclerosis and peripheral
lymphoid response57.
4) Adenocarcinoma
Gross: Poorly circumscribed with irregular infiltrative borders. The C/S is tan and
solid, with areas of haemorrhage or necrosis.
Microscopy: Resembles gastro-intestinal carcinoma with mucin production and even
signet ring cells. Tumours are characterized by glandular or ductal structures with
variable organization. The glandular structures are composed of nondescript cuboidal
cells58
5) Malignant mixed tumours - Includes:
a) A neoplasm with the basic pattern of mixed tumours, but in which all the
epithelial elements are malignant.
b) A true carcino-sarcoma where in both a carcinoma and recognizable
mesenchymal malignancy co-exists.
c) A metastasizing benign mixed tumours.
d) Carcinoma occurring in or in association with recognizable benign mixed
tumours.
First three are rare and most cases designated malignant mixed tumours
represent carcinomas arising in benign mixed tumours. Carcinoma arising in mixed
tumours comprises about 7 - 17% of parotid malignancies.
Gross: Tumour may be obviously invasive or may grossly resemble a circumscribed
benign mixed tumour. Necrosis, haemorrhage and cyst formation is common.
66
Microscopy: There is histological evidence of destructive and infiltrative growth of a
malignant neoplasm and there is pre-existing neoplasm with the features of a benign
mixed tumour. The malignant component may be characteristic of adeno-carcinoma,
squamous cell carcinoma or undifferentiated carcinoma54.
6) Epithelial-Myoepithelial Carcinoma:
• They are more common tumour of low-grade malignancy mainly seen in the
parotid gland. The cells form ball-like or trabecular clusters and are both basaloid
with scanty cytoplasm and myoepithelial with abundant pale, vacuolated
cytoplasm. Nuclei are mildly atypical with a pale chromatin and discrete central
nucleoli. Hyaline stromal material is present60.
7) Basal Cell Adenocarcinoma:
This accounts for 1% of all malignant epithelial tumours of salivary glands.
These tumours occur in adults. Age ranges from 27 to 92 years with an average age of
60 years. There is equal sex distribution for these tumours. Parotid gland is the most
common site.
Gross: These tumours are firm and range in size from 1.7 to 7cm, in longest
dimension and cut surface, shows uniform tan to gray white surface, often with a
coarse and fine nodularity.
Microscopy: The tumour is composed of various sized nests of cords of cells, a
histological appearance similar to that of basal cell adenoma. However, unlike basal
cell adenoma, the tumour grows in an infiltrative, destructive fashion. Necrosis and an
increased mitotic rate are also seen in some cases. Perineural and intravascular
invasion may be seen.68, 69
67
8) Sabaceous Carcinoma:
These tumours composed of variably sized nests or sheets of sebaceous cells.
The cells show different degree of maturity, pleomorphism, nuclear atypia and
invasiveness. Cellular pleomorphism and cytological atypia are uniformly present and
they are more prevalent than in sebaceous adenomas. The tumour cells have
hyperchromatic nuclei and are surrounded by abundant clear to eosinophilic
cytoplasm.61
9) Papillary Cystadenocarcinoma
These are rare tumours; the commonest sites of involvement are major
salivary glands. Age ranges from 20 to 86 years and average age is 54.7 years. Males
and females are equally affected.
Gross: These tumours are usually encapsulated, but may range from being
encapsulated to being invasive. Cut surface, shows cystic areas. Lesions may be
unicystic or multicystic, which range in size from 0.4 to 6cm.
Microscopy: Tumour is composed of large cystic spaces lined by epithelium that
often exhibit a papillary growth pattern. The cells lining the cystic spaces vary from
tall columnar to cuboidal to simple squamous and may be mucous secreting. Tumours
may have areas of clear, oncoccystic basaloid features. The papillary features are
common. The Lumina are often filled with mucus. Haemorrhage and dystrophic
calcifications are sometimes evident focally.61, 67
68
10) Oncocytic Carcinoma:
This neoplasm is one of the least common of all the salivary gland
malignancies. It represents only 5% of oncocytic salivary gland neoplasm and 0.05%
of all epithelial salivary gland neoplasms. Age ranges from 29 to 91 years with an
average age occurrence of 64 years. There is a male predilection for these tumours.
Gross: Tumour size ranges from 0.5 to 8 cm with infiltration into surrounding
structures.
Microscopy: Tumours are composed of large polyhedral to round cells having
eosinophilic, granular cytoplasm. These are arranged in an alveolar or synctial pattern
and sheets or in cords. There is a much greater degree of nuclear and cellular
pleomorphism and the number of mitotic figures is greater than that found in benign
oncocytoma. Non encapsulation and vascular or neural invasion or both may be
noted.61, 67
11) Salivary Duct Carcinoma:
The incidence of salivary duct carcinoma is difficult to assess because most of
the published surveys of salivary gland tumours do not include this specific category
of tumour. These neoplasms have a predilection for older patients with a male
predominance. The parotid gland is the commonest site.
Gross: These tumours vary in size from less than 1 cm to greater than 6 cm in
diameter and are usually yellowish grey to gray white. Sometimes they are
multinodular but these tumours are usually infiltrative and poorly circumscribed.
69
Microscopy: histological features show resemblance to that of ductal carcinoma of the
breast. Tumour cells are arranged in nests or cords, composed of atypical cells usually
containing abundant eosinophilic cytoplasm that form back to back glands and often
exhibit cribrifom, papillary or solid patterns.61
12) Adenocarcinoma, Not Otherwise Specified (NOS):
It affects patients primarily in the 4th to 8
th decade of life. Over 75% of
patients are between the ages of 40 to 79 years. Mean and median ages of the patients
are 55.6 and 58.6 years respectively. There is a male predilection. Major salivary
glands are involved in 66.2% of cases and minor salivary glands in 33.8%. Parotid
gland is the most common site.
Gross: A firm to hard mass replaces glandular parenchyma and compresses
surrounding tissue. Normally . Borders are irregular and often indiscernible from
surrounding tissue. Tumour invasion into the muscle and bone may be recognised.
Cut surface is white or yellowish white and may reveal focal areas of haemorrhage
and necrosis.
Microscopy: The histological diagnosis of adenocarcinoma, NOS depends more on
the exclusion of other characteristic types of salivary carcinomas than on the
recognition of histomorphological features that are specific to adenocarcinoma, NOS.
The cells in some of the tumours have abundant cytoplasm with distinct cell borders
and focally resemble myoepithelial cells. However, in other tumours, cells are closely
packed together with indistinct cell borders. Tumour cells are arranged in different
70
patterns varying from islands, anastomosing cords to diffuse, sheet like patterns with
variable amounts of intervening connective tissue.
The common pattern in adenocarcinoma, NOS is glandular or duct like
structures. The tumours may range from low to high grade.70
13) Malignant Pleomorphic Adenoma:
Malignant pleomorphic adenomas of salivary origin are relatively uncommon
neoplasm.
Malignant pleomorphic adenomas include three different clinical and
pathological entities.
a) Carcinoma Ex pleomorphic adenoma (carcinoma arising in a pleomorphic
adenoma)
b) Carcinosarcoma (true malignant pleomorphic adenoma)
c) Metastasizing pleomorphic adenoma
The first accounts for most of the malignant pleomorphic adenomas and
second and third are extremely rare. These tumours constitute approximately 12% of
malignant salivary gland tumours and 3.6% of all salivary gland neoplasms.72, 73
a) Carcinoma Ex Pleomorphic Adenoma:
These tumours accounts for 95% of all malignant pleomorphic adenomas and
6.5% of all malignant tumours. They occur in the 6th to 8
th decade of life with the
mean age of occurrence being 56 years. These tumours are common in females.
Gross: In general size varies 1.5 to 2, 5 cm in greatest dimension. Usually, these
tumours are poorly circumscribed and many extensively infiltrative. Occasionally,
71
they may be encapsulated or well circumscribed. Cut-surface shows white or tan-gray
colour and are hard in consistency.
Microscopy: Most of the tumours are composed of typical benign pleomorphic
adenoma with only small foci of carcinomatous tissue. Malignant areas in carcinoma
ex pleomorphic adenoma consist of epithelial cells with an increased nuclear
cytoplasm ratio, prominent nucleoli and increased number of mitotic figures. The
most common histological patterns in these areas are poorly differentiated
adenocarcinoma or undifferentiated carcinoma. Destructive infiltrative growth is the
most reliable histological criterion for the diagnosis of carcinoma ex pleomorphic
adenoma.
b) Carcinosarcoma:
This is also known as true malignant pleomorphic adenoma. It is a tumour in
which both the stromal and epithelial components fulfil histological criteria of
malignancy.
Gross: The majority of carcinomas are grossly infiltrative with poorly defined
margins. Occasionally, tumours are partially or totally encapsulated. Tumours range
in size from 2 to 9cms in greatest dimension. Cut surfaces are usually greyish in
colour and occasionally areas show cystic change, haemorrhage and calcification.
Microscopy: Each of these tumours is biphasic, with varying proportions and types of
sarcomatous and carcinomatous elements. Sarcoma is the dominant tissue in the
majority of tumours with chondrosarcoma being the commonest. Tumours may
72
manifest areas of osteo sarcoma, fibro sarcoma, high grade sarcoma and malignant
fibrous histiocytoma.
c) Metastasizing Pleomorphic Adenoma:
It is common of the three types and is a neoplasm in which both the primary
salivary gland tumour and its metastatic lesions are composed of typical benign
appearing pleomorphic adenoma. Earlier literature has referred to these tumours as
“benign metastasizing mixed tumours”. 67, 70
14) Squamous Cell Carcinoma:
In one of the first comprehensive review of tumours of salivary glands in1953,
Foote and Frazell reported 39 primary squamous cell carcinomas.
Squamous cell carcinoma represents 1.6% of all primary epithelial salivary
gland tumours. 4.4 % of malignant epithelial tumours and 6.9% of all major salivary
gland epithelial malignancies. Most cases occur between 7 to 65 years.
The mean and median ages are 60.5 and 64.6 years respectively and range is 7
to 95 years. There is a 2 to 1 male predilection. It accounts for 6.3% of parotid, 8.3%
of submandibular and 3% of sublingual epithelial malignancies.
Gross: these tumours are unencapsulated, poorly demarcated and firm to hard in
consistency. Cut surface is light gray or white.
Microscopy: These tumours are similar to squamous cell carcinoma from other sites,
ranging from low grade, highly keratinised neoplasm to poorly differentiated sheets of
tumour cells with minimal keratinisations. Adjacent soft tissue invasion and regional
metastasis are common. Trabaculae of desmoplastic fibrous connective tissue often
73
separate the tumour into multiple nodules. Islands of squamous cell carcinoma
occasionally have marked infiltrates of lymphoid tissue in close apposition.59, 67.
15) Small Cell Carcinoma
Small cell carcinomas are extremely rare and account for less than 1% of
major salivary gland tumours, but they account for 2.8% of minor salivary gland
tumours. They are common between 5th and 7
th decade of life. There is a male
predominance. 85% of the small cell carcinomas arise from parotid glands and
remainder from submandibular gland.
Gross: the tumour margins are usually poorly demarcated with infiltrating edges and
rarely circumscribed. These tumours are firm to hard in consistency. Cut surface
shows variegated appearance.
Microscopy: The tumours are composed of infiltrating large sheets, ribbons, cords or
nests of anaplastic cells. The tumours cells sre round to oval in shape, having minimal
cytoplasm with hyper chromatic nuclei containing finely dispersed chromatin and
inconspicuous nucleoli.67, 71, 72
16) Other Tumours:
a) Undifferentiated carcinomas:
These are uncommon tumours and account for 0.4% of all salivary gland
tumours and 1to 4.5% of all the malignant parotid tumours. Parotid gland is the most
common site followed by submandibular gland. Minor salivary gland origin is
extremely rare.
74
Typically they demonstrate increased mitotic figures with a significant degree
of cellular pleomorphism. Because of the bizarre cells and the lack of organization
into a recognizable arrangement, there is great difficulty is distinguishing the origins
of the tumour, thus it is placed into the undifferentiated category.
b) Malignant lymphoma:
Primary malignant lymphoma of salivary glands is rare and virtually always
occurs in parotid gland, divided into 2 sub groups:
1. Arising in the intra parotid and Para parotid nodes,
2. Salivary parenchyma.
Primary nodal lymphoma presenting as a parotid lesion is often a stage I lesion
and is associated with a good prognosis. Parenchyma lymphomas usually arise in the
setting of lymphoepithelial lesions with or without Sjogren’s syndrome62.
c) Metastatic Carcinoma:
Reach the gland by direct spread, lymphatic or haematogenous spread.
Malignant melanoma and squamous cell carcinoma of the mucosa of the upper aero-
digestive tract via the lymphatic’s account for 80% of the parotid metastasis.
Haematogenous spread is most often from carcinoma of the lung, kidney, breast and
colon63.
COMMON SOFT TISSUE TUMOURS OF THE SALIVARY GLANDS
1) Haemangioma:
Haemangioma accounts for 50% of all parotid tumours in children. It is
uncommon in other salivary glands and in adults. The capillary haemangioma are
75
probably neoplasm or vascular malformations, where as the cavernous haemangioma
are best regarded as reactions to trauma or else vascular malformations. The capillary
haemangioma show the modest female predominance. 61% are present at birth and
86% appear within the first month
Gross: of an excised specimen of a capillary haemangioma reveals a spongy purple
lobular mass, which infiltrates the gland.
Microscopic: Shows endothelial proliferation with vascular differentiation, which is
the hallmark of this disease. There are solid masses of cells and multiple anatomising
capillaries surrounding the acini and ducts. Microscopic examination of cavernous
haemangioma reveals dilated blood vessels and sinuses lined by endothelium. It is un-
encapsulated and infiltrating.73, 74
2) Lymphangioma:
Lymphangiomas (cystic hygromas) were first recognised as being of
lymphatic origin in1828. These vascular malformations not true neoplasm. Salivary
gland involvement is very rare, 50% present at birth and 80 to 90% manifest by
second year of life.
Gross: Reveals a spongy, cystic multi-loculated lesion containing fluid that is either
cloudy or yellow tinged.
Microscopy: Demonstrates endothelial lined spaces with a connective tissue
stroma73,74
.
76
3) Lipoma:
Lipomas are uncommon and account for 0.6 to 4.4% of all parotid tumours.
They are less common in the submandibular gland. They most commonly occur in the
fifth to sixth decades and are rare in children.
Gross: Reveals them to be smooth well demarcated and yellow.
Microscopy: shows them to be composed of mature fat cells with an enveloping
capsule. In pure form, fatty infiltration is referred to as lipomatosis. Glands displaying
acinar cell hypertrophy with or without fatty changes have been called sialosis,
sialoadenosis or nutritional mumps74.
4) Neurofibroma:
This tumour also arises from the Schwann cells but behave much differently.
This may be solitary or part of neurofibromatosis. They are usually present as
encapsulated lobulated swelling.74
Salivary Neoplasm in Children:
Salivary neoplasm in children is rare. They constitute less than 5% of all
salivary tumours, 50% are benign. Among these, pleomorphic adenoma and
Warthin’s tumour are common.
Based on an institutional data from 1990 to 1997 Brandon G. Bentz et al,
indicates that less than 5% of the neoplasm, benign or malignant present in patients
who are 16 years of age or younger. Several features distinguish the neoplasm in this
age group, as compared those in adults:
77
• A much greater frequency of non epithelial tumours, parotid haemangioma are
most common.
• Preponderance of parotid gland involvement ex: 7:1 with submandibular
glands74,75
TUMOURS OF MINOR SALIVARY GLANDS
Tumours of the minor salivary glands comprise less than 2% of all tumours of
the head and neck, and 37% to 48% of these arise from the palate. Minor salivary
gland tumours have also been described in the upper lip, buccal mucosa, pharynx,
larynx, nasal cavities, and sinuses. Minor salivary gland tumours of the hard palate
have a propensity to arise at the junction of the hard and soft palates, followed by the
hard palate.
Age and Sex Incidence:
• There is a slight preponderance of lesions in females, with a peak incidence in the
third through the fifth decades. Despite their relative rarity among head and neck
neoplasm, minor salivary gland tumours continue to generate notable academic
interest, likely due to their potential for aggressive behaviour.
Histology:
• Adenoid cystic carcinoma, adenocarcinoma, and mucoepidermoid carcinoma have
each been proffered as the most common malignant tumour of the palatal minor
salivary glands. Other malignant tumours encountered include low grade
polymorphous adenocarcinoma, carcinoma ex pleomorphic, acinic cell carcinoma,
and undifferentiated carcinoma.
78
• The majority of benign minor salivary gland tumours of the palate are
pleomorphic adenomas, with scattered monomorphic adenomas and basal cell
adenomas reported with the incidence ranging from 33% to 70% of all tumours113
.
CLINICAL FEATURES
The appearance of a lump in or near the salivary glands is the most common
mode of presentation which may or may not be associated with pain.
The salivary gland swellings can be presented as acute inflammatory
condition, chronic inflammatory condition, calculus diseases, a benign or malignant
tumours, manifest as congenital abnormalities or represent involvement of systemic
disorders of various salivary glands. So the clinical features of these are considered
individually76, 54, 39
.
1. Acute Suppurative Sialadenitis:
The clinical presentation of acute salivary infection is sudden onset of pain
and swelling overlying the affected gland. it most commonly affects the parotid gland.
Examination reveals indurations, erythema, edema and extreme tenderness
over the affected gland. Intraoral Stensen’s or Wharton’s ducts may appear
erythematous or inflamed, and massage of the affected gland may express pus from
the ductal orifice. The pain is exacerbated on attempting to drink or eat. There is
associated malaise, pyrexia and often regional lymphadenopathy. Affected gland will
become fluctuant after abscess formation38, 77
.
79
2. Chronic Recurrent Sialadenitis:
Chronic recurrent sialadenitis may follow an acute of suppurative sialadenitis.
The recurrent attacks of pain and swelling usually associated with eating and drinking
and accompanied by the discharge of flecks of pus in the saliva. The disease is much
more common in the parotid salivary gland.
Physical examination confirms the tender enlarged swellings and massage of
the gland often produces scanty saliva at the duct orifice39, 38, and 77
.
3. Sjogren’s Syndrome:
It is an autoimmune disease, the symptoms and signs were first described by
Hadden in1883.Sjogren’s syndrome has been classified into primary and secondary.
Sjogren’s syndrome described by Sjogren’s in 1933 comprises a triad of dry
eyes, dry mouth and rheumatoid arthritis. The combination of dry eye and dry mouth
but without connective tissue disorder is known as primary Sjogren’s syndrome. The
combination of dry eye, dry mouth and rheumatoid arthritis is called as secondary
Sjogren’s syndrome38, 78
.
4. Granulomatous Diseases:
They may occur with or without systemic manifestations. Generally both
parotids enlarge simultaneously, and submandibular, sublingual and lachrymal gland
may involve. Granulomatous disease may present as
a. Mycobacterium infections: presenting as tumour like swelling with little pain.
b. Cat scratch disease: In these condition children is mostly affected. Cervical
lymphadenitis and mild pyrexia is present which is self limiting.
80
c. Actinomycosis: presents as a firm, indurate mass with a draining fistula containing
sulphur granules.
d. Syphilis: diagnosis is established by serology.
e. Toxoplasmosis: presents as necrotizing granulomatous inflammation and various
systemic fungal infections38, 78, 79, 80
.
5. Viral Infections:
Mumps is the most common viral disease to involve the salivary glands. It is
commonly recognised in the 4 to 6 year old age group. The incubation period is 2 to 3
weeks
Clinical onset is characterised by pain and swelling in one or both the parotids.
Systemic symptoms include fever, malaise, myalgia and headache and usually resolve
before the parotid swelling. One episode of infection confirms lifelong immunity38.
6. Sialolithiasis:
Calculi may form in any of the salivary glands. The submandibular gland is
the most common (80%), parotid gland (20%) followed by sublingual glands and
minor salivary glands (1-2%) follow at a lower rate of recurrence.
Commonly, the patient gives a history of recurrent swelling and pain in the
involved gland, usually associated with eating. With repeated episodes, infection may
intervene. Occasionally patient will present with a stone that is palpable in the
salivary duct without any history of salivary swelling or inflammation.
Physical examination reveals diffuse enlargement and tenderness of the
involved gland. The calculus is frequently palpable. Calculus within the duct tends to
be irregular38, 81
.
81
7. Cystic Lesions:
Congenital cysts usually manifests immediately after birth or in the
childhood. Presents as a fluctuant swelling both in the floor of the mouth and in the
submandibular triangle.
Acquired cysts are usually dominated by the clinical features of the causative
agent such as calculus, neoplasm, trauma, parotitis etc82.
8. Sialadenosis:
Painless diffuse enlargement of the salivary glands, either unilateral or
bilaterally, most commonly associated with metabolic disorders, nutritional
deficiencies and reaction to some drugs. Parotid gland is involved commonly43.
9. Mucoceles:
Male-to-female ratio of occurrence is 1:1.3. Ranulæ tends to occur most
frequently in the second and third decades of life, with an age range of 3 - 61 years.
Ranulæ are usually either one-side or the other in the floor of the mouth and 2
- 3 cm in diameter. Occasionally, they extend across the whole of the floor of
the mouth. A ranula is most commonly observed as a bluish cyst located below the
tongue. It may fill the mouth and raise the tongue. Typically, these are painless
masses that do not change in size in response to chewing, eating or
swallowing but may interfere with these functions (speech
or chewing / eating). Occasionally, pain may be involved.
82
10. Clinical Features Of Salivary Neoplasm
Clinical feature of salivary neoplasm can be described under following
headings.
1) Rate of growth of the swelling: The average duration before seeking treatment is
described as 4-5 years by different authors for a benign tumour. The duration in
carcinoma is in months rather than years. The rate of growth varies greatly from
tumour to tumour and even in the same tumour from time to time.
2) Pain: benign tumours of the salivary glands are painless. Pain is the most
presenting symptom in cases of malignant tumours. Sudden onset of pain in a
mixed salivary gland tumours always denotes some complication like malignancy.
Pain is of dull, boring when present. It is usually localized to the region of the
tumour. Sometime pain may be referred to the corresponding ear, along the
branches of auriculotemporal nerve.
3) Facial palsy: Facial nerve is never involved in benign tumours, however large the
tumour may be. Involvement of the facial nerve in the course of mixed tumours
always indicates a malignant change. In cases of carcinoma the most striking and
important clinical manifestation is facial palsy. But absence of facial palsy does
not rule out possibility of the tumour being malignant. The incidence of facial
nerve weakness at the time of presentation in patients with parotid malignancies
ranges from 10-15%.
4) Ulceration: benign tumours never ulcerate. Ulceration of benign tumours occurs
when they turn malignant or when some counter irritant applied to the tumours. In
the advanced cases of carcinoma, skin may be fixed, reddened, and give rise to
ulceration
83
Signs of Salivary Tumours:
1. Swelling: The characteristic features of the swelling are globular or ovoid in
shape, well defined margins; surface is lobular and nodular in some cases. Rarely
the swelling may be diffusing in parotid gland and submandibular gland tumours,
whereas it is common feature in sublingual and minor salivary glands. The
swelling is usually mobile. Look for fluid in middle ear and/ or medial
displacement of the tonsil by parapharygeal space involvement. In carcinoma of
salivary glands, the tumour is rapidly growing, hard, and irregular in outline with
nodular surface.
2. Local invasion: In advanced carcinoma, skin may be fixed, reddened and give
rise to ulceration. Tumour is often fixed to the underlying deeper structure
(external auditory canal, mastoid tip, zygomatic arch, mandible, masseter muscle,
pterygoid muscles or sternomastoid). The TM joint should be examined for signs
of direct tumour extension. The mastoid tip must be palpated to determine
whether there may be difficulty freeing the tumour from this structure. Fixation to
the tip will likely change the scope of the surgery and should be identified pre-
operatively so that radiological imaging can be undertaken to further define the
extent of the invasion. Parotid neoplasm may involve the ear canal secondarily
via the fissures of santorini. Even when the skin is intact, there may be subtle
signs of subcutaneous invasion such as oedema or indurations of the canal skin.
3. Nodal involvement: Regional lymph nodes are never enlarged in benign tumours,
lymph node metastasis occur when these turn malignant, commonest lymph node
that are enlarged are upper deep cervical group, submandibular and sub mental
group. Regional metastasis correlates strongly with a diminished overall
survival86.
84
4. Oral cavity examination should include inspection of duct opening for evidence
of abnormal or purulent drainage. These findings are more often associated with
inflammatory disease. Trismus should be identified because it may be indicative
of invasion of the masseter or pterygoid muscles. The oropharynx must be
carefully evaluated for signs of parapharyngeal space involvement. Typically this
will be manifested by a sub mucosal bulge in the soft palate or tonsillar regions83.
A complete head and neck examination is essential. The salivary gland may
be involved with another malignant process e.g. malignancy from a local skin cancer
(squamous cell carcinoma or melanoma) or cancer in the oropharynx or nasopharynx.
Malignancy below clavicle can present as metastasis in the parotid gland years after
the initial disease (e.g. breast, lung and kidney). Note: non-Hodgkin’s lymphoma is a
likely diagnosis in elderly83, 84, 85
.
Clinical feature of specific neoplasms:
A. Pleomorphic adenoma:
This is the commonest benign salivary gland tumour and is virtually the only
benign neoplasm to occur in submandibular, sublingual and minor salivary glands. PA
present as slow growing painless mobile, firm and circumscribed mass. When it arises
in the deep lobe of the parotid gland it may present as parapharygeal mass. There is
seldom any compromise of 7th nerve. Most tumours are located in the tail of the
parotid gland, although they can involve other parts of the gland. 10% of the PA
occurs in the deep lobe of the parotid gland. Incidence of recurrence after
parotidectomy in PA is 5%.
Incidence of malignant transformation is 3 - 15%. Except for recurrence
prognosis is excellent. Recurrence in PA may be due to (1) Inadequate surgery
85
(Enucleation) (2) Inadvertent spillage (3) Tumour removal with inadequate margin (4)
Multicentricity11.
B. Warthins tumour:
WT present as well defined, soft to firm mass. It is usually asymptomatic.
However, 18% of patients in the series complained of pain, and there has been one
report of facial paralysis. Characteristically arises in the inferior pole of the parotid
gland and occasionally originates in the lymph nodes adjacent to that part of the
gland. This tumour scans ‘hot’ with technetium51.
C. Oncocytoma:
It accounts for less than 15% of all salivary gland tumours. It usually occurs in
the parotid gland and is quite unusual elsewhere. It presents as well defined, lobular
mass with firm to hard consistency. In reported series, bilaterally and multi-centricity
have been conspicuous. Most tumours occur in the 6th decade. There is 2:1 F: M ratio.
This is one of salivary gland tumours that scan ‘hot’ with technetium53.
D. Mucoepidermoid tumour:
Attention is usually drawn to a painless solitary enlargement of the body or
tail of the parotid gland or the submandibular gland. Duration usually averages less
than 1 year.
The tumour is relatively well circumscribed and movable, and it may mimic a
mixed tumour. Pain, facial paralysis, and fixation to the overlying skin are not
common but when present are usually harbingers of high grade lesions. High-grade
tumours have a high recurrence rate (15-75%)57.
86
E. Acinic cell tumour:
Tumour growth is usually slow; rarely may they have a more rapid
enlargement. Pain or tenderness is experienced frequently. Facial nerve paralysis is
infrequent but is an ominous prognostic sign. It is generally regarded as a low-grade
malignancy87.
F. Adenoid cystic carcinoma:
Typically it grows slowly. Pain and tenderness generally occur during the
course. Fixation to skin and the surrounding deeper structures develops in the later
stages. Regional lymph nodes involvement is found in 10-15% of cases. Distant
metastasis to lung and bone occurs late in the course of the disease56.
G. Adenocarcinoma:
About 25% of patients complain of the effects of the nerve involvement.
Facial nerve irritability occurs first and muscle spasm can be produced if the tissues
over the nerve are trapped. A few patients present with skin involvement. The risk of
lymph node metastasis is 24 - 36%70.
H. Malignant mixed tumor:
Long history of slow growing parotid swelling, with recent rapid growth
brings them to medical attention. Pain, skin ulceration, facial nerve weakness,
attachment to skin, and telangiectasia can occur and should lead the clinician to
suspect malignancy in a mixed tumour. The most frequent symptom is painless mass.
15% of patients note recent rapid growth, occasionally with ulceration. Pain has been
87
described in 4 to 55% of patient, and appears to be more common in submandibular
gland tumours52.
I. Miscellaneous malignant tumours:
a) Squamous cell carcinoma: It grows rapidly and half of the patients have
metastatic lymph node involvement at the time of presentation. It causes pain,
facial nerve paralysis, commonly associated with early skin fixation and
ulceration59.
b) Malignant lymphoma: Primary lymphomas are uncommon. Occur in the 5-
6th decade of life, F>M, H/O Sjogren’s syndrome or arthritis is elicited in
majority of patients. They run an indolent clinical course where as lymphoma
arising in intra salivary gland lymph nodes usually present as rapidly enlarging
swelling within the gland62.
c) Undifferentiated carcinoma: they are highly malignant. Approximately 33%
have partial or total facial paralysis 40% beyond the parotid on presentation.
13% present with regional metastasis61.
J. Tumours of Minor Salivary Glands:
Most of the tumours are detected by the patient as an asymmetric swelling of
the palate; sometimes tumours are completely asymptomatic and were detected only
on routine dental examination. Other symptoms encountered included pain,
ulceration, and dysesthesias.
A painless swelling of the palate is the most common presenting symptom for
tumours of the palatal minor salivary gland tumours. Both pain alone and neural
88
complaints including pain and dysesthesias exhibit a statistically significant
association with a histopathologic diagnosis of adenoid cystic carcinoma.
Most of the tumours of minor salivary glands are usually found on the hard
palate or at the junction of hard and soft palate, often extending to the greater palatine
foramen. Most of the tumours are well circumscribed with central ulceration
indicating prior biopsy or central tumour necrosis.
Malignant tumours sometimes present with extension to involve one or more
of the several surrounding structures including the maxillary alveolous, tonsil,
nasopharynx, and sinonasal cavities. Extensions are also seen to the submucosa of
nasal floor or the maxillary sinus112, 113,114.
Some common soft tissue tumour of the major salivary gland:
a) Haemangioma (capillary or cavernous): most often presents during childhood
and accounts for almost half of the hamartomatous and neoplastic parotid lesions
seen in this age group. The capillary haemangioma are far more common. There is
modest female preponderance. 61% present at birth and 86% appear within 1
month. They appear as a discrete mass of variable consistency and growth rate,
during the period of rapid growth. The mass is generally painless, does not trans-
illuminate, no bruit74.
b) Lymphangiomas are painless, trans-illuminate, and usually slowly enlarging.
50% of them present at birth. There is an equal sex distribution74.
c) Schwannoma, neurofibromas are slowly growing tumours with an equal sex
distribution. Paraesthesias are common, it is tender, 50% of these have facial
weakness when seen74.
89
Figure 23: A Photograph Showing Intraoral
Salivary Calculi
Figure 24: A Photograph of Female Patient with Left Pleomorphic
Adenoma Presenting as Only Swelling
90
Figure 25: A Photograph of Male Patient with Left
Submandibular Sialolithiasis
Figure 26: A Photograph Female Patient with Right Parotid
Swelling with Deep Lobe Involvement and Skin Changes and Ear
Lobe Elevation
91
Figure 27: A Photograph of Female Patient with Left Parotid Swelling
and Ear Lobe Elevation
Figure 28: Photograph Showing Mucous Retention Cyst in the Mouth
92
DIFFERENTIAL DIAGNOSIS
1. Sialadenosis is the term used for non inflammatory and non neoplastic Salivary
gland enlargement. When the tumour begins it is very difficult to Differentiate
from calculus disorders, inflammation etc, especially when these are Unilateral
and small.
2. Enlarged lymph nodes within the parotid gland or cervical region may be
mistaken for a gland tumour. Hence, it is very important to examine all the
drainage areas, to rule out any other cause.
3. Lipomatous pseudo hypertrophy of a gland can be mistaken for a tumour. This
happens because of infiltration of the gland by fatty tissue.
4. Masseter hypertrophy can mimic parotid gland tumours. But the rhomboid shape
of the masseter which is wide above than below is unmistakable and it hardens on
clenching the teeth. This condition affects young males, and is often self limited.
It can cause pain and trismus. Malignant hyperthermia which has a mortality of
80% can occur in this condition, especially provoked by anaesthetic clinically.
5. Facial nerve neuroma is a rare cause for swelling in the parotid region.
6. Infra-temporal fosse tumours can mimic deep lobe tumours of the parotid and can
be differentiated from it only by imaging studies.
7. Torus palate can be mistaken for minor salivary gland tumours.
93
TNM STAGING OF SALIVARY GLAND TUMORS (1997):88
Proposed staging system for major salivary gland cancers by American joint
committee For Cancer Staging (AJCC).
T Primary tumour
TX Primary Tumour cannot be assessed.
T0 No evidence of Primary Tumour.
T1
Tumour 2 Cm or less in greatest dimension without extraparenchymal
Extension.
T2
Tumour more than 2 cm but not more than 4 comes in greatest dimension
Without extraparenchymal extension.
T3
Tumour having extraparenchymal extension without seventh nerve
involvement and / or more than 4 cm but not more than 6 cm in greatest
Dimension.
T4
Tumour invades base of the skull, seventh nerve and / or exceeds 6 cm in
Greatest dimension.
N Regional lymph nodes.
Nx Regional lymph nodes cannot be assessed.
No No regional lymph node metastasis.
N1
N1Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest
Dimension.
N2
N2a Single ipsilateral node >3 cm, <6cm in diameter.
N2b Multiple ipsilateral node, none >6 cm.
N2c Bilateral or contra lateral nodes, none >6 cm.
N3 Metastasis in a lymph node more than 6 cm in greatest dimension.
M Distant metastasis
Mx Distant metastasis cannot be assessed.
M0 No distant metastasis.
M1 Distant metastasis.
94
Stage Grouping
Stage I
T1 N0 M0
T2 N0 M0
Stage II T3 N0 M0
Stage III T1 N1 M0
T2 N1 M0
Stage IV
T4 N0 M0
T3 N1 M0
T4 N1 M0
Any T N2 M0
Any T N3 M0
Any T
Any N M1
INVESTIGATIONS
Acute inflammatory conditions generally can be diagnosed by history and
physical examination alone, whereas chronic inflammatory diseases, granulomatous
disease and neoplastic disorders require supplemental diagnostic information
including laboratory tests, imaging studies, or biopsy54.
With careful history and physical examination, it is not difficult to diagnose a
case of salivary gland swelling. Apart from the routine blood examinations, the
following investigations are commonly used for diagnosis of salivary swellings89, 90
.
1. Plain x ray
2. Sialography
3. Radiosailography
4. Ultrasonography
5. Computed tomography
95
6. Magnetic resonance imaging
7. FNAC, Biopsy
1. Plain X Ray:
• Most submandibular calculi are radio opaque and about 94% can be diagnosed by
the plain x ray taken in intra oral view. Stones in the superior gland or proximal
Wharton’s duct may be hard to visualise on plain lateral projections radiographs
because the stones may be superimposed on the teeth or mandible. Often, an
anteroposterior view with the mouth open will allow visualisation.
• Parotid stones are more likely to radiolucent and nearly 40% can be diagnosed by
plain X ray
• It is very uncommon for the patients to have a combination of radio opaque and
radiolucent stones. Still some calcifications in the area can confuse the diagnosis
like phleboliths, calcified cervical lymphadenopathy and arterial atherosclerosis of
the lingual artery.
• X-ray current usefulness is essentially limited to involvement of radio opaque
calculus. Any areas of calcification in the major salivary gland and also is useful
for malignant tumours which are fixed to bone (Thickening of the mandible) and
infiltrate intracranial producing facial palsy43, 81
.
2. Sialography:
Sialography is currently used to evaluate calculi, obstructive disease,
inflammatory lesions, penetrating trauma and mass lesions. Sialograms are reported to
be 100% effective in detecting ductal and intraglandular calculi.
96
Equipment:
To perform a sialogram, the following equipment should be available, water
soluble contrast media, such as meglume diatrizote 76%,a good light source, a topical
anaesthetic for ductal orifice, lachrymal dilators, a lachrymal cannula ,a syringe,
polyethylene tubing, a Rabinov cannula, and a tapered side hole needle.
USE:
It helps in detection of occlusion of the duct, a salivary cutaneous fistula or a
salivary oral fistula or development of a sialocele.
Disadvantages:
• It may cause infection or inflammation
• Extravasations of the dye may result in severe inflammatory reaction preventing a
clear demarcation of clear tumour margin and may also delayed the planned
surgical procedure and high pressure generated during the procedure disseminates
the tumour cells.
Contraindications:
• Acute sialadenitis and in patients with allergy to iodine2.
3. Radio Sialography:
Current radioactive scanning of the major salivary glands is done with
technetium the tetra-oxygenated form-pertechtenate. Radio isotope scanning is used
for evaluation of the parenchymal function and detects mass lesions. It is used for
detecting mass lesions of the parotid and submandibular gland. Scanning has little to
97
offer in the evaluation of the sub lingual and minor salivary glands. The scan should
be performed in the resting state because uptake in the parotid is greater42, 43
.
4. Ultrasonography:
Bozin et al (1971) first reported the use of ultrasonography to study the
salivary glands. High resolution ultrasound (7.5-10 MHz) helps in differentiating
intra-glandular from extra-glandular tumours and benign from malignant tumour,
where in benign show variable reflectivity with well defined borders and malignant
tumour show low reflectivity with poorly defined border, Inflammatory lesions show
high reflectivity with diffuse borders. In a study from Spain, specificity And
sensitivity for malignancy was 96.4% and 81.8% respectively obtaining similar results
with other authors. Also used to delineate whether the mass is cystic or solid.
Ultrasound imaging also helps in direct needle aspiration of parotid abscess. It
is also used to localise the calculus. As many as 90% of the stones greater than 2mm
in size can be detected as an echo dense spot in an ultrasound2, 91
.
98
Figure 29: x-ray of submandibular calculi
Figure 30: Sialogram Showing Stricture of Submandibular
Duct
99
5. Computed Tomography
CT has largely replaced other diagnostic studies for the study of salivary
masses, since 1979, when it was first introduced.
CT scans delineate solid from cystic masses and can detect masses as small as
1cm within the substance of the salivary glands. The anatomic delineation of a mass
involving any of the salivary glands can be well defined by ct scanning.
Benign masses within the parotid gland often have smooth well defined
birders on ct scans. Aggressive and infiltrative malignant neoplasms often have
diffuse borders and may show adjacent bone destruction or invasion of adjacent
tissues.
CT scans is especially useful in differentiating deep lobe tumours from
parapharyngeal masses.
Byrne MN et al. Studied that CT scans of 110 resected parotid masses shows
following characteristics:
a) For tumours with well defined borders, homogenous appearance and high signal
density, the Diagnosis will more likely a benign tumour or a low grade malignant
tumour.
b) For tumours with ill defined borders ,heterogeneous appearance and high density,
the diagnosis will more likely a high grade malignant tumour.
c) Ill defined borders, heterogeneous appearance and mixed signal density will be
consistent with an inflammatory process.
This is a valuable supplement to MRI in evaluating the bone adjacent to
tumour. CT combined with sialography is excellent for differentiating intrinsic from
extrinsic masses, benign from malignant masses, superficial from deep lobe tumour
and showing the relationship of the mass to the facial nerve2, 38, 91, 90
.
100
6. Magnetic Resonance Imaging:
It is superior to CT for better identification internal architecture of the gland
and better definition of tumour border. It provides direct multi-planar imaging without
the need for contrast agents and ionizing radiation. Recent advances in MRI are
gadolinium (a Para-magnetic compound enhances vascular lesions) and MRA.
The contrast between the tumour and surrounding tissue is greater than with
CT scanning but tissue details are less well defined.
• It helps in differentiating benign from malignant nature of salivary tumour by
knowing margin (smooth/infiltrative), solid/cystic, necrosis or hemorrhagic areas
within the tumour and malignant tumour show gadolinium enhanced images.
• Deep lobe tumour of parotid can be differentiated from a parapharygeal mass,
wherein later shows fatty plane all around, but parotid tumour shows attachment
to the superficial lobe. Also helps in differentiating postoperative fibrosis from
recurrent nodules.
• In case of malignant tumour it shows involvement of carotid artery or other
structure that indicate inoperability. Demonstrate whether facial nerve
compression or invasion.
• MRI is the investigation of choice in cases of ranula to know it’s origin
Disadvantage:
• It does not show stone and bone. Many attempts to determine benign from
malignant nature have shown misdiagnosed interpreting benign as malignancy
(CT-39% and MRI-35%). The consensus is that MRI cannot be used confidently
to distinguish benign and malignant masses28, 44, 65, 76
.
101
Indication of CT/MRI:
• Malignant or recurrent tumours
• Large neoplasm
• Suspected carotid artery involvement
• Involvement of local structure (including nerves which may suggest
inoperability).
7. Radio-nucleotide scan (PET)
It is done using technetium 99m (t1/2 is 6½). Scan performed in resting state
because uptake in parotid is greater. Little useful in other salivary glands. Warthins
and oncocytoma show hot spots. Also helps in differentiating benign from malignant
tumour on basis of malignant lesions having higher metabolic rate and increased
incorporation of radio-labelled deoxy-glucose than benign lesions.
8. CT Sialography
It is found that useful in tumour mapping preparation for surgery. Specifically
the tumours location in relationship to deep lobe, facial nerve and the Para pharyngeal
space can be assessed. CT sialography cannot definitely diagnose or rule out the
malignancy to avoid the need for surgery92, 93
.
102
Figure 31: Ultrasound Of Warthin’s Tumour
Figure 32: CT Scan Of Mucoepidermoid Carcinoma
Of Right Parotid
103
9. Biopsy
FNAC:
It is a simple and reliable method for obtaining the tissue diagnosis of salivary
gland Swellings. The diagnostic accuracy with regard to the benign versus
malignancy is about 98% for benign salivary gland swellings, 93% for primary
malignant salivary gland swellings, and 88% for metastatic tumours.
This helps in proper counselling of patient regarding surgery and preoperative
evaluation which will vary according to whether the mass is primary, neoplastic or
lymphoma or metastasis. If malignancy is found, further imaging can be done and non
neoplastic causes of salivary swelling can be treated without surgery.
Figure 33: MRI of Pleomorphic Adenoma Of Left
Parotid
104
Advantages and Uses:
1. FNAC is usually an office procedure. It is less laborious and cost effective.
2. It is safe, less traumatic and better tolerated by the patients.
3. It is rapid and results are available in less than 20-30 min and the procedure can be
repeated as often as necessary.
4. In certain tumours the smears can be easier to interpret than histological sections.
5. It produces enough cellular material for various auxiliary studies (DNA,
molecular analysis and immunohistochemistry studies).
Complications of FNAC:
There is a possibility of lymphatic, haematogenous and canalicular
dissemination. But this does not have any clinical implication. Several studies have
failed to report any such cases. Infection is minimal due to aseptic precautions.
Limitations:
1) Specific diagnostic conclusions may not always be reached. Aspirates from MEC,
Lymphoma and sometimes PA also give some diagnostic difficulties
2) Definitive diagnosis is not drawn if the sample is inadequate or the representative
area is not aspirated properly.
3) Practice and skill in aspiration techniques are necessary.
4) Experience is required for accurate interpretation.
5) Diagnostic information is limited.
• Sensitivity is 93.3-95.7% (98% for benign; 93% for primary malignancy; 88% for
metastatic tumour).
105
• Specificity is 98-100%. Lay field et a land Young GA et al found high diagnostic
efficiency of FNAC in Salivary gland tumours.
Open biopsy: is rarely performed because of risk of injury to facial nerve and tumour
implantation and tumour recurrence with both benign and malignant tumours. As a
result of high diagnostic Accuracy of FNAC open biopsy is almost contraindicated
now days.
Frozen section: evaluation of efficacy and usefulness of frozen section study yielded
Varying results. It is utilized to assess the margins of resection94, 95, 96, 97, 98
.
TREATMENT:
Management of the salivary gland swelling depends on the pathology of the
swelling. Treatment of Inflammatory and non inflammatory, non neoplastic disease of
the salivary glands is dependent upon the diagnosis and includes antibiotics,
supportive therapies, symptomatic management, and Surgical and non surgical
interventions. Whereas the surgery is the mainstay of treatment of both Benign and
malignant salivary gland tumours. Adjuvant radiation therapy is administered in
selected malignant salivary gland tumours and chemotherapy may have palliative
benefit in uncontrolled malignant neoplasm38, 54, 85
.
Treatment of Inflammatory and Non Inflammatory Non-Neoplastic Diseases:
1. Acute Suppurative Sialadenitis:
Treatment of the acute sialadenitis is directed at reversal of the underlying
medical condition responsible for infection. If the patient presents at an early stages
106
before abscess formation, the infection can usually be controlled by anti-biotics, warm
packs and rehydration. Incision and drainage is advised if infection does not subside
with in 48 hrs with a small incision taken over the most prominent part of the
swelling, usually incisions are taken superficially and parallel to the facial nerve
branches, pus is drained out by a sinus forceps and the wound is loosely approximated
over a drain.post-operatively antibiotics is based on culture and sensitivity of the
pus38, 99
.
2. Chronic Sialadenitis:
Chronic sialadenitis is more common in submandibular salivary gland and the
capacity of the gland to recover is usually is very poor following infection, the gland
itself should be removed38, 99
.
3. Sjogern’s Syndrome:
Treatment of Sjogren’s syndrome remains largely empirical and symptomatic,
and no clinical trial has been proved capable of changing the course of the disease.
Patients with keratoconjunctivitis should avoid windy or dry climates, dust or
smoke. Oral hygiene after meals avoidance of sugar containing foods is important for
the prevention of dental disease. Artificial tears are essential to protect cornea
Pilocarpine hydrochloride a saliva secretogauge (5mg 3-4 times a day) can be
administered for the treatment of xerostomia. Patients are advised to carry water
bottles for frequent drinks.
Diuretics, antihypertensive drugs and anti depressants should be used with
care38, 100
.
107
4. Granulamatous Disease:
Granulamatous disease should be treated according to the pathology and
moreover some of them are self limiting and resolve without treatment38.
5. Mumps:
Treatments of viral salivary gland infection are primarily supportive, including
rest and adequate hydration, because the disease is self limiting.
The most significant advancement in the treatment of mumps is prevention in
the form of vaccination commonly combined with measles and rubella vaccine. A
single subcutaneous dose after 12 months of age confers lifelong immunity77.
6. Sialolithiasis:
The anatomy of the salivary glands and it’s ducts is very pertinent to
determine the mode of therapy for sialolithiasis.
Submandibular stones are treated surgically either through a transoral
sialolithotomy approach or through a complete sialaldenectomy through a extra oral
approach. If the stones are palpable it can be removed via Trans oral route, especially
anterior stone which are palpable. For very anterior stone filleting the submandibular
duct is considered the best approach. This can be done under a topical or local
anaesthesia.
Stones in a slightly more anterior position may be amenable to modification of
trans oral.Approach where the stone is cut down directly. Deeper submandibular
stones are generally removed through sialadenectomy.
108
Parotid stone management is more problematic, parotidectomy remains the
mainstay of surgical management of the majority of the stones.
Extracorporeal lithotripsy is a new modality that was introduced iin the early
1980s and has revolutionised the treatment of urinary stones. Iro H et al (1989) first
reported the use of extracorporeal lithotripsy for the parotid stones. Extracorporeal
lithotripsy can be performed without the need for local or general anaesthesia.
Extracorporeal lithotripsy appears to be the most effective for the treatment of parotid
stones compared to submandibular stones38, 85, 42, 1o1
.
7. Cystic Lesions:
True cysts are more common in the parotid. The cysts may be acquired or
congenital. Excision during a quiescent period with preservation of the facial nerve is
curative77.
8. Sialadenosis:
Mechanism of asymptomatic enlargement of parotid gland is unknown. The is
generally good if the underlying disease can be corrected and the parotid gland
generally returns to normal43.
9. Salivary Gland Tumors
Treatment
• Treatment is challenging because of their infrequency, their unpredictability and
varied Biological behaviour and their prolonged risk of recurrence.
In formulating a treatment plan, following factors should be kept in mind that
may affect Prognosis68:
109
1. Histopathological diagnosis.
2. Lymph node metastasis.
3. Facial nerve paralysis.
4. Skin involvement.
5. Recurrent tumour.
6. Distant metastasis.
7. Irradiation sensitivity.
SURGERY
Surgery is the main stay of treatment for salivary gland tumours, both benign
and malignant. Surgery For salivary gland tumours never really developed until
World War II Due to fear of injuring the Nerves and partly also due to the ever
present risk of spreading infection along facial planes, during the pre-antibiotic era.
• Principles of surgery on salivary gland tumour:
• “Removal of entire tumour mass should be achieved in toto, without breaching
capsule or producing spillage.”
• “The integrity of important nerves should be maintained when practicable. We
have to identify facial nerve and its branches by meticulous dissection”.
• “Avoidance of parotid duct injury which may lead to salivary fistula” 28, 102, 103,
104.
Surgery tor Parotid Gland
Pre-Operative Preparation:
� Counselling the patient regarding transient or permanent facial nerve paralysis
done at time of admission and prior to surgery.
110
� Written consent: It is a good principle to explain the possibility of the nerve injury
to the patient prior to the surgery on salivary gland.
� Pre-anaesthetic evaluation
� 0.5 ml of TT injection.
� Tab. diazepam 5mg and H² blocker previous night.
� Nil by mouth for 10 hours.
� Preparation of operative field- cleanly shaved about 5cm around external ear in all
direction.
Anaesthesia:
General Anaesthisia by endotracheal tube is mandatory. This follows the
usual sleep dose of Thiopentone and succinylcholine. Preference should be given to a
relaxant intermittent positive pressure respiration technique, which removes any
possibility of straining with its attendant Congestion during the course of operation.
Anaesthesia in maintained with vecuronium and Halothane. This produces a mild
degree of hypotension, which is advantageous as it decrease the Operative bleeding.
Despite the apnoea produced by these two drugs, there is still sufficient tone in The
facial muscles to respond to the surgeon’s use of a nerve stimulator during the parotid
Dissection.
Position of the Patient:
The patient in supine, head is turned to opposite side with the neck Extended.
Head end is raised by 15º to decrease venous engorgement. The external acoustic
meatus is plugged with sterile cotton; towels are placed exposing the side of the face,
to note Twitching, while operating.
111
Procedures:
1) Superficial parotidectomy:
Definition:
Superficial parotidectomy involves removal of only superficial lobe of the
parotid gland.
Indication: All benign parotid tumours confined to superficial lobe.
Technique:
A lazy ‘S’ incision (Sistrunk’s or Patey’s or Modified Blair incision) is made, the
parotid gland is Exposed. Some surgeon employ a ‘Y’ shaped incision, wherein
the two limbs of the Y straddling the pinna. Incision made through skin,
subcutaneous tissue down to the platysma muscle in cervical region and to the
parotid fascia in the preauricular region. The incision begins opposite the tragus in
Front of the ear and curves around, the lobule of the ear in facial lobar crease to
reach the mastoid;
Post operative distortion of the ear lobule minimized by allowing 2-3 mm of skin
to stay with the Lobule.
From there the incision gently curves down in the second upper cervical skin
crease as far as the tip of the hyoid bone, at the level of the sternomastoid muscle
maintaining two finger breadth Distances from inferior border of the mandible to
avoid transecting the marginal mandibular nerve.
Gentle curve at the post-auricular component of the incision is essential to prevent
necrosis of skin Flap. The incision is usually begun from the lower part for the
convenience, so that blood from the Upper part of the incision does not obscure
the vision.
112
Skin flap is elevated from postero-inferior to antero-superior direction, leaving a
thin layer of fat Over the parotid fascia and platysma muscle. The postero-inferior
flap is reflected off the mastoid Process and upper fibres of the sternomastoid
muscle in order to expose the thin lingula of the Parotid tissue that overlaps these
structures. The anterior skin flap is raised as far as the anterior Border of the
gland, Superior flap, including the lobule of the pinna is reflected upwards as far
as The cartilaginous plates, which form the floor of the external auditory canal.
Elevation of the flap is continued until entire gland is exposed. Caution must be
exercised as the anterior border of parotid Gland is approached, because the
branches of facial nerve become superficial at this point.
The greater auricular nerve is seen running up from the middle of the posterior
border of the Sternomastoid muscle to the pinna, parallel to the external jugular
vein. It is divided or retracted.
Mobilization of the posterior part of the gland by dissection with scissors begins
with elevation of the lingula of parotid tissue in order to expose the mastoid
process and tendinous attachment of sternomastoid muscle. The lingula can be
lifted forwards with mosquito artery forceps provided that they do not impinge on
the tumour. Absolute haemostasis should be maintained with diathermy so that
bleeding does not interfere with recognition of the facial nerve. The gland is
mobilized down to the level of the posterior belly of the digastric muscle where
the styloid process can be felt deep to this muscle.
The space between the tail of the gland and the external acoustic meatus is
developed to expose the facial nerve. The main trunk of facial nerve is identified;
the upper and lower divisions and the named branches are exposed by tunnelling
along each in turn. A pair of mosquito forceps is well suited to this purpose.
113
Tunnelling must be done with care and the communicating tissue between
superficial and deep parts of the parotid divided successively within the field of
vision produced by this manoeuvre. This allows the superficial parotid tissue to
be lifted away gradually exposing the full anatomical distribution of the facial
nerve. Meticulous haemostasis must be maintained at all times in order to allow
identification and visualization of the branches of the nerve. Dissection is
continued as far as the anterior border of the gland, when the whole superficial
lobe can be removed. Finally, the parotid duct is ligated and transected. After
removal of the tumour, haemostasis is achieved carefully with bipolar cautery.
Suction drain placement and pressure dressing then is applied to prevent
postoperative Hematoma102, 103, 104
.
2) Conservative Superficial parotidectomy:
Definition:
A conservative parotidectomy is defined as any procedure that is less than a
classic superficial parotidectomy, and where less than a full facial nerve is dissected.
Indications:
Conservative parotidectomy with appropriate postoperative radiotherapy may
be an acceptable procedure without potential morbidity, such as postoperative facial
palsy, in the treatment of low-grade parotid cancers confined to the superficial lobe if
the facial nerve is sufficiently distant from the tumor115
.
114
3) Total conservative parotidectomy:
Definition:
This involves removal of both the outer and inner parts of the parotid salivary
gland, which are separated by the nerve that moves the face, whilst avoiding damage
of this nerve.
Indications:
1. Conditions involving the deep lobe or both the outer/ superficial and the deep part
of the gland:
• Usually benign deep lobe pleomorphic adenoma or large dumb bell shaped
pleomorphic adenomas involving both lobes.
• Recurrent pleomorphic adenoma.
• Malignant parotid neoplasms without preoperative facial nerve palsy and
where tumour can be separated off from the nerve.
• Small intraglandular deep lobe malignant tumours.
• Other benign progressive conditions involving the whole gland such as
recurrent severe suppurative parotitis secondary to intraglandular stones or
ductal narrowing.
2. Conditions requiring access to deep structures whilst preserving the facial nerve,
eg, parapharyngeal space or infratemporal fossa tumours not involving the facial
nerve.
Technique:
In this both lobes, superficial and deep are removed leaving the facial nerve
intact. The steps of the surgery are identical to the previous procedure of superficial
conservative parotidectomy. At the completion of removal of the superficial lobe, the
115
facial nerve is lifted up with a nerve hook or latex sling gently and by a combination
of sharp and blunt dissection the deep lobe is removed. The blood vessels namely the
external carotid and the external jugular vein are doubly ligated inferiorly and their
branches superiorly to minimize bleeding.116
4) Total Radical Parotidectomy:
Definition:
Involves removal of both the outer and inner part of the parotid salivary gland
(which are separated by the nerve that moves the face) as well as the facial nerve. A
neck dissection may be performed at the same time.
Indication:
• Preoperative facial nerve palsy.
• If intra-operative evidence of gross infiltration or encasement of nerve by the
tumor, even in presence of normal preoperative facial function.
• Recurrent pleomorphic adenoma after repeated revision operations where nerve
goes through recurrent tumour.
• Conditions requiring access to deep structures where preservation of the facial
nerve is not possible, eg, parapharyngeal space or infratemporal fossa tumours.
Technique:
Entire parotid gland is removed along with the facial nerve. The trunk of the
facial nerve or its main upper and lower divisions are isolated and divided.
Preservation of the first division of the facial nerve facilitates subsequent repair by
grafting, provided that it does not prejudice removal of the tumour. Markers either by
black silk ligatures or silver clips can aid identification after excision has been
completed. The parotid gland and the tumour are dissected forwards off the masseter
116
muscle and capsule of the TM joint. The termination of the external carotid artery is
found as it winds round the posterior border of the vertical ramus of the Mandible. It
is divided and ligated at this level as also its branches as they are encountered. Large
Venous tributaries, which follow the posterior facial vein, must be similarly dealt
with.
Parotid duct may be recognized as its turns medially to penetrate the muscles
of the cheek where it may be formerly ligated. If the parotid duct is involved, it may
be excised with cuff of muscle and mucosa. The mucosa is closed with interrupted
chromic catgut sutures. The transition from the substance of the parotid gland to the
fascia of the cheek and fibro fatty tissue is recognized easily and excision of the gland
is completed by dividing the remaining soft tissue attachment.
Shaheen advocated transmandibular approach for very large deep lobe
tumours of the parotid by osteotomising the mandible and reaffixing it after the
procedure. For malignant tumors infiltrated deeply, the pharyngeal serosa and
pterygoid muscle are removed102, 103, 104
.
5) Extended Radical Parotidectomy:
Definition:
This includes all the components of a total radical parotidectomy, as well as
adjacent structures involved with disease. This may involve bone (lower jaw, jaw
joint, mastoid), muscle (from the neck and face) and cartilage from the ear canal.
Total radical parotidectomy involves removal of both the outer and inner part of
the parotid salivary gland (which are separated by the nerve that moves the face)
as well as the facial nerve. A radical or modified radical neck dissection is usually
performed at the same time.
117
Indications:
• Conditions involving the deep lobe or both the outer/ superficial and the deep part
of the gland, as well as adjacent structures.
• Recurrent pleomorphic adenoma after repeated revision operations where nerve
goes through recurrent tumour and involves adjacent structures such as skin,
muscle and cartilage.
• Malignant parotid neoplasms with preoperative facial nerve palsy and where
tumour cannot be separated off from the nerve and involves adjacent structures.
• Malignant neoplasms of adjacent structures involving all of the parotid gland
including facial nerve, eg, malignant middle ear or mastoid tumours.
• Malignant tumours requiring access to deep structures where preservation of the
facial nerve is not possible eg parapharyngeal space or infratemporal fossa
tumours.
Technique:
Technique is same as total radical parotidectomy along with resection of the
skin, mandible, muscle and temporal bone as determined by the extent of resection of
the primary lesion, with primary reconstruction followed by post operative
radiotherapy. Skin defects must be repaired using either local random flap, provided
they give sufficient area or regional axial flaps for larger defects117
.
Facial nerve identification during parotid surgery:
The most constant landmark for the facial nerve is at the stylomastoid
foramen, between the styloid and mastoid process. During routine parotidectomy,
however, complete access to this region is difficult. The following landmarks and
techniques can be used for identification of the facial nerve.
118
� 1cm deep, 1cm inferior and 1cm anterior to triangular end of tragus called trigonal
pointer.
� More constant landmark is tympano-mastoid suture line. It is a groove that is
easily Palpated between mastoid and tympanic portions of the temporal bone.
Nerve exits from stylomastoid foramen 6-8 mm medial to suture line.
� The posterior cephalic margin of the posterior belly of digastrics and its
attachment to mastoid has been used to identify the trunk. The Nerve is
approximately 1.5 cm antero-cranial to the point.
� The base of the styloid process is 5 to 8 mm deep to the tympanomastoid suture
line.
� The facial nerve lies on the posterolateral aspect of the styloid process near its
base.
� Retrograde technique- it is abandoned. The cervical branch of the facial nerve
located lateral to the posterior division of the retromandibular vein. Tracing the
external jugular vein superiorly to the posterior division of the retromandibular
vein will lead to the point where the cervical branch crosses the vein. The
marginal branch can be found crossing the facial vein by tracing the vein
superiorly from the neck. The buccal branches (present 1cm below the zygoma)
can be identified with careful dissection near the Stensen’s duct and it lies just
superior to the ducts. The zygomaticotemporal branches can be identified as they
ascend over the zygomatic arch midway between the tragus and lateral cantus of
the eye, and anterior to the superficial temporal artery. These branches can be
traced proximally to the by use of nerve stimulator104, 105
.
119
Surgery for the Submandibular Gland
1. Total excision:
Indication: All benign and malignant tumours of submandibular gland.
Technique:
Under general anaesthesia, with patient positioned same as for parotid surgery,
drapes are placed to expose the operating field. Two inch long upper cervical skin
crease incision, which begins two finger breadths (3 cm) from the lower border of
mandible and at point two inches anterior to angle of mandible. The incision is
deepened by cutting the platysma and the deep fascia, at one stretch and the superior
flap is reflected upwards, to protect the marginal mandibular nerve which is present in
the flap. The marginal mandibular nerve will course superficial to the submandibular
gland fascia and under the platysma muscle, usually above the inferior border of the
gland. The cervical branch of facial nerve at the angle of mandible is also not
disturbed, as the incision is anterior to this. Alternatively the marginal mandibular
nerve can be preserved if facial vein is identified, ligated and transected, while
incising the submandibular gland fascia at inferior border of gland.
Dissection continues to free the submandibular gland from the surrounding
tissue off the underside of the mandible and anterior part of the gland is now
mobilized by dissecting it from the mylohyoid muscle. The facial artery is seen on the
deeper aspect of the posterior superior part of the gland where it is ligated and divided
and the gland is freed, the facial artery is once again ligated at the anterior border of
the masseter. The superficial lobe is fully free.
A hook is placed under the posterior border of the mylohyoid muscle which is
retracted medially and anteriorly, and by blunt dissection the deep lobe is also
removed, taking care not to damage the lingual nerve above and the hypoglossal nerve
120
below. The duct is traced forwards as possible, ligated and divided. Surgery is now
complete. The wound is closed in two layers, first the platysma and then the skin after
keeping a drain in dependent part38, 102, 103
.
2. The commando operation:
Indication:
Malignant submandibular tumour which is fixed to the mandible with cervical
lymph node metastasis.
Technique:
Submandibular gland is removed as per the above procedure along with the
part of the involved mandible and the enlarged lymph node106
.
Surgery for the Sublingual Gland
1) Treatment of Ranula:
a) A few cases of mucoceles and ranulas spontaneously resolve, especially in
infants and young children. If symptoms are minimal in this young age group,
aspiration of the lesions and periodic follow-up for 6 months have been
suggested as an alternative to surgery.
b) Mucus extravasation phenomenon: Surgical excision of the mucocele along
with the adjacent associated minor salivary glands is recommended. The risk
for recurrence is minimal when appropriate surgical excision has been
performed. Aspiration only of the mucocele's contents often results in
recurrence and is not appropriate therapy, except to exclude other entities prior
to surgical excision.
121
2) Marsupialization of the oral ranula with packing of the entire pseudocyst with
gauze for 7-10 days. The entire ranula is unroofed, and the packing material is
firmly placed into the entire cavity of the pseudocyst. This technique allows for
re-epithelialization of the pseudocyst cavity; seals the mucinous leak; and
provokes a foreign body inflammatory reaction, leading to fibrosis and atrophy of
the involved acini. The procedure may be effective with the sublingual gland
because it has multiple draining excretory ducts. If this does not eliminate the
ranula, additional surgical therapy is initiated with removal of the ranula and the
offending major salivary gland.
Surgery of Minor Salivary Glands:
Histological diagnosis Treatment
Pleomorphic adenoma Excision with 1-cm clinical margin at its periphery
including epithelium and periosteum
Monomorphic adenoma Conservative local excision includingmargin of
normal uninvolved tissues
Adenocarcinoma Wide excision and adjuvant radiotherapy
Adenocystic carcinoma Wide excision and adjuvant radiotherapy
Mucoepidermoid carcinoma Wide excision and adjuvant radiotherapy
The treatment of choice of minor salivary gland neoplasm is surgery. Surgical
approach to these tumours depends on the site and histology of the tumour. Neck
dissection are recommended for clinically positive necks and in those with high grade
tumours. Similarly radiation is used as adjuvant therapy in high grade tumours.
122
• Low grade malignant tumours of the palatal mucosa such as pleomorphic
adenoma and low grade mucoepidermoid carcinoma and adenocarcinoma ia
usually treated by a soft tissue excision with documented margins of 1 cm
clinically uninvolved tissue around it’s periphery and including the palatal
periosteum followed by healing by secondary intention, palatal perioteum serves
as an effective anatomical barrier, the palatal bone is not excised even if cupped
out pressure resorption has taken place.
• Malignant tumours of the palatal mucosa such as intermediate and high grade
adenocystic carcinoma, wide excision in the form of partial or hemimaxillectomy
is done followed by radiotherapy for high grade lesions. Chemotherapy coulad
also be used as an adjuvant112,113,114
.
Management of the Neck Node:
Comprehensive neck dissection either a MRND or RND is indicated when
there are clinically positive nodes. Armstrong and associates in 1992, suggested
elective treatment of neck in patient with
• High grade tumours of any size or low grade tumours of at least 4 cm in size.
• Dissecting level I, II and III to identify occult disease106
.
Postoperative management:
• Patient is examined in immediate postoperative period for facial, lingual and
hypoglossal nerve function.
• Administration of analgesics for 3 days and antibiotics for 5 days.
• Postoperative mouth wash/ gargle decrease the chances of infection from oral
cavity.
123
• Drainage tube is removed on 2 or 3 days.
• Sutures removed on 5 day102, 103, 104
.
COMPLICATIONS OF SURGERY
The complication of salivary gland surgery can be summarized as follows:
Early Late ( After 6 Months)
1. Injury to the nerves
2. Haemorrhage\hematoma
3. Salivary fistula\ sialocele
4. Infection
5. Necrosis of skin flap
6. Seroma
7. Trismus
8. Frey’s syndrome
9. Hyperasthesia of the local
skin
10. Cosmetic deformity
11. Hypertrophied scar
12. Recurrence
1. Injury to the Nerves
a) The marginal mandibular nerve is the Commonest to be injured at surgery
for parotid gland and submandibular gland, because it is thinner Than other
branches and also it is more vulnerable, due to its proximity to surgical
incisions. An Injury of this nerve produces drooping of the lower lip on the
same side. This is called “wry neck”.
b) Greater auricular nerve injury results in numbness of pinna, but some
amount of recovery takes Place due to overlapping by the surrounding sensory
nerves in the neighbourhood. Recovery will take 6-9 months to occur. a small
area of skin may remain anaesthetized. Some Authors recommend
preservation of the posterior branches of the greater auricular nerve to achieve
faster and more complete recovery in sensory function 8.
124
c) Lingual Nerve can be injured during surgery on the submandibular gland very
rarely; this causes ipsilateral anaesthesia of the tongue. Still rarer is injury to
the hypoglossal nerve, causing deviation of the tongue onto the same side.
d) Facial Nerve: Post-operative facial nerve dysfunction involving some or all of
the branches of the nerve is the most frequent early complication of parotid
gland surgery.
Temporary facial nerve paresis, involving all or just one or two branches of
the facial nerve, and permanent total paralysis have occurred, respectively, in 9.3% to
64.6% and in 0% to 8% of parotidectomies, reported in the literature. The cases of
transient facial nerve paresis generally resolved within 6 months, with 90% within 1
month. Temporary paresis usually resolves, according to Laccourreye, within the
18thpost-operative month.
The incidence of facial nerve paralysis is higher with total, than with
superficial parotidectomy, which may be related to stretch injury or as result of
surgical interference with the vasa nervorum. Revision parotidectomy or
parotidectomies for parotid fistula are generally associated with a higher incidence of
facial weakness. The branch of the facial nerve most at risk for injury during
parotidectomy is the marginal mandibular branch. Older patients appear to be more
susceptible to facial nerve injury.
Temporary facial nerve weakness is a cosmetic problem, and patients should
be told their appearance will return to normal. However, eye protection must be
ensured. If facial paresis causes incomplete closure of the eye, the patient must be
advised to use ophthalmic moisture drops frequently during the day and an
ophthalmic ointment and eye protection at night. Regular follow-up with an
125
ophthalmologist is mandatory . Moreover, use of botulinum toxin to induce temporary
ptosis avoids the need of surgical tarsorrhaphy118
.
Owen ERT, 1989 reported 9% incidence of permanent facial paralysis and
38% of temporary facial Paralysis107
. Nerve function usually returns within 3-6 month
but may take up to a year.
Facial nerve reconstruction
A number of procedures are available to treat this, both nerve repair and
plastic surgical correction. If nerve is cut, cut ends are identified, it is best to perform
an end to end anastomosis, at the same sitting. If there is gap in the nerve, Facial
nerve reconstruction- cable nerve grafting using greater auricular nerve/ sural nerve to
bridge the defect is the standard procedure done at time of the surgery. A Hypoglossal
nerve transposition (XII-VII graft) can also be tried; temporalis and masseter muscle
transfer are other alternatives118
.
2. Haemorrhage and hematoma:
As the operative site is dependent area, collection of serum and blood is not
infrequent. Rarely bleeding may be from slipped legation of branch of facial artery or
anterior facial vein. Collection is aspirated daily and pressure dressing applied until it
ceases. Significant bleeding is best avoided by careful dissection, isolation and
legation of the vessels. Incidence of hematoma varies from 0.8-16% following
parotid gland surgery.
126
3. Frey syndrome
The best described and more frequent complication following parotidectomy
is gustatory sweating or Frey syndrome.
Pathogenesis:
The pathogenesis of Frey syndrome is based on the aberrant regeneration of
sectioned parasympathetic secretomotor fibres of the auriculotemporal nerve with
inappropriate innervation of the cutaneous facial sweat glands that are normally
innervated by sympathetic cholinergic fibres.
Clinical Features
Frey syndrome is a disorder characterized by unilateral sweating and flushing
of the facial skin in the area of the parotid gland occurring during meals that becomes
evident usually 1-12 months after surgery. The clinical incidence of Frey syndrome,
after parotidectomy, has been reported, in various studies, to be as high as 50%
(severe in 15%). Gustatory sweating is detected in almost 100% of cases, evaluated
by means of a post-operative iodine-starch test (Minor test).
Treatment: Treatment is reassurance and conservative management
Many surgical and non-surgical attempts have been made to prevent the
clinical appearance of Frey’s syndrome.
� Systemic or topical application of various anticholinergic agents (scopolamine,
glycopyrrolate, diphemnanil-methylsulfate) and the use of stellate ganglion
blockade have been unsuccessful.
127
� Surgical treatment has included cervical sympathectomy, tympanic neurectomy,
sternocleidomastoid transfer and dermis-fat grafts and the use of various
materials, as interpositional barriers, but the outcome of these techniques has been
disappointing since only temporary relief is achievedgc. Better results have been
reported with some prophylactic measures, including the use of the superficial
musculoaponeurotic system (SMAS) as a flap or the superficial temporal artery
fascial flap. These techniques aim to create a physical barrier between the divided
fibres of the auriculotemporal nerve and the sweat glands in the facial skin.
� More recently, good results have been obtained with local injection of botulinum
toxin (BTX) .In patients affected by gustatory sweating, a Minor test is performed.
The total amount of drug used for treatment depends, of course, on the surface
area of sweating.. BTX treatment has always been well tolerated without needing
anaesthesia. The gustatory sweating usually ceases in the treated area, within 48-
72 hours. only transient paresis of the orbicularis oris, in very few cases, has been
reported in literature . A marked long-lasting improvement, ranging from 11 to 36
months after a single injection, has also been described.
� In summary, it can be concluded that Botox A injection is a safe and effective
method and the treatment of choice for patients with extensive gustatory sweating.
At present, BTX therapy is considered the gold standard for curative treatment of
Frey syndrome118
.
128
4. Parotid Fistula and Sialocele
Definition:
A parotid fistula is a communication between the skin and a salivary duct or
gland, through which saliva is discharged. Parotid salivary fistula is a relatively
common complication after parotidectomy.
Pathogenesis:
Salivary fistula or sialocele occurs if the resected edge of the remaining
salivary gland leaks saliva and drains through the wound or collects beneath the flap
(sialocele). Flow through the fistula increases during meals, particularly during
mastication. In dubious cases, analysis of the fluid can confirm parotid secretion due
to high amylase content.
Wax and Tarshis, in 1991, reported an overall post-parotidectomy fistula rate
of 14%, Laskawi et al. described persistent parotid fistula in 4% of patients following
parotidectomy .
Computed tomography fistulography can be performed to look for the extent
of the fistula
Types
a) Caused by the opening of Stenson’s duct
b) Sinus tracts originating in the glandular structure
Treatment
a) Aspiration and pressure dressings
b) Anti-Sialogogues
129
c) Radiation therapy
d) Parasympathetic denervation ( Tympanic Denervation)
e) Cauterization of the Fistula
f) Reconstruction of the duct
g) Superficial or total parotidectomy with tract
Conservative management
• A conservative modality is based on the regular aspiration of the content and
compression dressing. This mode of treatment is mainly employed in sialocele.
Anti-cholinergic agents are used to suppress the glandular function during healing
or in an attempt to close a fistula or a sialocele. Propantheline bromide is
commonly used.
• Radiation Therapy is especially considered for refractory salivary fistulas. It
induces fibrosis and atrophy of the gland. Approximately 1800 rads for more than
6 weeks is required.119
Surgical Therapy:
Surgical excision of the fistulous tract followed by right pressure dressing of
the wound is an effective management option.
Three operative techniques are described
1. Repair of the duct over a stent
2. Ligation of the duct
3. Fistulisation of the duct into the oral cavity
130
Tympanic neurectomy:
Para-sympathetic secretomotor fibres carried to the gland from the inferior
salivary nucleus via the tympanic plexus to otic ganglion. Supplied to the parotid
gland by the auriculaotemporal nerve. Trans tympanic sectioning of the jacobson’s
nerve by drilling into the temporal bone at hupotympanum is done. Glandular atrophy
occurs in 6 months. High failure rate was seen due to varied anatomy of the nerve
reinnervation.
Botulinium Toxin Injection:
Staffieri et al. first proposed, in 1999, BTX in the treatment of salivary fistula
and sialoceles after conservative treatment failure.
Fistulas and scialoceles are managed with botulinum toxin injection after
conventional conservative management techniques fail. The residual substance of the
gland is injected percutaneously with a total of 10-20 mouse units (U) of BTX-A
(Botox, Allergan) in two-three spots. The botulinum toxin injection is performed on
an outpatient basis with little discomfort for the patient. The localised cholinergic
block achieved with botulinum toxin injections, avoids the side-effects caused by
systemic anticholinergic drugs and avoids surgical risks. Inhibition of parotid
secretion leads to a temporary block in salivary flow followed by glandular atrophy,
thus allowing healing of the fistula118
.
5. Cosmetic deformity:
Barely noticeable scar is possible with placement of the incision in skin fold.
Another source of aesthetic concern is the depression or hollow resulting from the
parotid gland resection, particularly following total parotidectomy.
131
6. Recurrence:
Occurs in both, benign and malignant tumour; may recur loco-regionally or
present as distant metastasis up to 20 years after assumed curative local treatment. In
case of pleomorphic adenoma recurrence has declined from the range of 20-30% to
0.7 %, as superficial parotidectomy has become the standard procedure.
Recurrence has to be excised surgically, for long term cure. There is no
evidence that radiotherapy/Chemotherapy affects survival after diagnosis of distant
metastases107, 102
.
RADIOTHERAPY
Major role is adjunctive to the surgery in form of postoperative radiotherapy,
improve survival and cure rates (Armstrong J.G.). This will decrease the recurrence
rate from 26.6 to 9.1% (Guilla mondegui O.M.1975). There are many reports of long
term control of large inoperable tumours by RT. So RT is indicated in all stage II, III,
IV (AJCC) and stage I with high grade.
• The indications for RT are: Postoperatively for all high grade tumors including
adenoid cystic carcinoma.
• Extra-parotid extension/perineural invasion (Locally advanced) - involvement of
skin, nerve and bone.
• Facial nerve involvement.
• Gross/microscopic residual disease
• For incompletely resectable disease, to treat the residual disease left behind in
presence of
The radiation dose is 6000cgy in 30 fractions is given over 6 to 7 weeks. In
tumour with close margin, dose is 6500cgy. When gross disease is present, then
132
7000cgy with a reducing field technique is required. When using a split course of RT,
give pre-operatively course of 4,000-4,500 CGY in 4weeks, then surgery is planned
for 6 weeks after pre-operative RT. Once the surgical scar has healed and the
patient’s general condition allows, the remaining 2,000-2,500 CGY are given to the
main volume.
ACC is poorly sensitive to RT; so adequate surgical excision is the main stay
of treatment. MEC are moderately sensitive but radio-curable, but others are fairly
sensitive to radiation but not radio-curable. In case of ADCC, the radiation field must
include the course of cranial nerves because peri-neural spread is common.
Lymphomas are extremely sensitive to RT103, 110
.
RT for inoperable tumour:
Aim is to irradiate the planned volume to 6,500 CGY in 6 - 7 weeks giving
daily Treatments of 200 CGY. Fast neutron RT provides higher rates of loco-regional
control of unresectable salivary gland carcinoma than photon or electron RT and it is
the initial.Treatment of choice. Only disadvantage is its lack of wide spread
availability103, 109
.
CHEMOTHERAPY
There is no established standard chemotherapy because of the lack of formal
trails with adequate number of patients. Indications are limited to diseases that are
metastatic or locally advanced and unresectable. The most commonly used drugs in
combination CT Are cisplatin, 5 Flurouracil & doxorubicin or 5-flurouracil,
adriamycin and methotrexate has given variable success in some cases111
.
133
Prognosis:
• Salivary gland tumors are known for late recurrence and hence long term follow
up is essential.
• The 5 year survival rate of the malignant tumors are as follows-
1. Low grade mucoepidermoid tumor 95%
2. Acinic cell tumor 75%
3. High grade mucoepidermoid tumor 50%
4. Malignant pleomorphic tumor 50%
• The five year survival rate for malignant pleomorphic arising denovo is 5% and
15 year survival is 1.5%.
• MEC of the low grade variety has the best prognosis and undifferentiated
carcinoma the worst prognosis.
• Distant metastasis occurs only on 20% of malignant salivary gland tumors.
Adenocystic carcinoma is known to recur even after 10 years.
134
Figure 35: Photograph Showing
Branches of Facial Nerve
Figure No 36: Photograph Showing Deep Lobe
of Parotid Gland With Facial Nerves
Figure 34: Photograph of Modified
Blair Incision
OPERATIVE PHOTOGRAPHS
135
Figure 37: An Excised Specimen of
Pleomorphic Adenoma of Parotid Gland
Figure 38: Photograph after the Wound
Closure of Superficial Parotidectomy
Figure 39: Photograph Showing Surgery of
Submandibular Gland
136
METHODOLOGY
This prospective study of consecutive cases of salivary gland swellings is
based on 40 cases admitted in various surgical units in J.J.M. Medical College and
Chigateri District hospital, Davangere, during the period from May 2009 to July 2011.
40 cases of salivary gland swelling are studied and data is presented here, which were
analyzed and conclusion drawn, presented in tabular form with explanatory notes
below each table. The statistics have been compared with different standard studies
conducted on same subject by various authors around world.
Inclusion criteria:
• All patients admitted to surgical wards of J.J.M. Medical College and Chigateri
District hospital with salivary gland swellings due to obstructions of the salivary
duct and neoplasia.
• Patients who are willing for investigation and treatment.
Exclusion criteria:
• All salivary gland swellings arising as a result of congenital conditions.
• Salivary gland swellings arising as a result of inflammation. (ex. Mumps,
Parotitis).
• Salivary swellings associated with systemic diseases. (Sjogren’s syndrome).
All patients admitted were evaluated by documenting the history, through
clinical examination, routine laboratory investigations and specific investigations. In
history, importance was given to presenting complaints, duration of lump, rapid
increase in size,associated symptoms of facial nerve involvement, previous surgical
137
treatment or any medical problem. Associated medical conditions like diabetes,
hypertension and anemia were managed and controlled before surgery with the
patient’s advice.
As a part of general work up of surgery in all patients, hemoglobin level,
bleeding time, clotting time, urine, sugar albumin, microscopy, chest screening, ECG,
Blood urea, serum Creatinine, RBS was estimated. Specific investigations like FNAC,
X-rays of Mandible were done for all patients in the study group. Ultrasound,
Sialography, C T Scan, MRI was not done for any of these patients in the study group,
as there was no facility for these investigations in the hospital and because of the poor
economic backgrounds of the patients.
After evaluation of the swellings by clinical examination and by specific
investigations, a surgical plan was formulated. The final decision was taken per
operatively by the surgeon. The required specimen was sent for histopathologocal
examinations. Appropriate antibiotics and analgesics are administered post
operatively for all cases. Drainage tube was removed when the drain was less than
20ml and sutures were removed on 5th day. Malignant tumors were referred to Kidwai
Memorial Institute of Oncology, after surgery, for post operative radiotherapy. The
adjuvant treatment was decided depending on the final HPE report.
Different modalities of treatment adopted in this study are
1. Surgery alone
2. Surgery and post operative radiotherapy
The follow up period of these patients ranged from 3months to 1 year. All
patients were asked for follow up after 15 days of surgery then every month for 1st
year then every 3 months in 2nd year, to detect morbidity and recurrence. Long term
follow up is necessary to study the actual prognosis of the patients and tumour
138
recurrence and to know the ideal mode of treatment for each condition which was not
possible in this study.
139
RESULTS
Table -1: Incidence of Salivary Gland Swellings at C.G. Hospital and Bapuji
Hospital
Year
Total No. of
surgical
admissions
Total No. of
salivary gland
swellings
Percentage
June 2009 To
May 2011
14863 40 0.27
Total number of admissions to the Department of General Surgery were
14863, 40 cases of salivary gland swellings were admitted during June 2009 to May
2011. This constitutes 0.27% of total admissions.
140
Table – 2: Age Incidence of Salivary Gland Swellings
Age in Years No. of
Patients Percentage
0-10 1 2.85
11-20 5 14.28
21-30 4 11.42
31-40 15 28.57
41-50 9 11.42
51-60 6 17.14
61-80 5 14.28
Total 40 100.0
In our study, age of the patients varied from 9 years to 80 years. Average age
of the patient was 40.6 years.
The case of lowest age group i.e., 9 years was of non inflammatory swelling
and the case of highest age i.e., 80 years was of tumor swelling.
2.85
14.28
11.42
28.57
11.42
17.14
14.28
0
5
10
15
20
25
30
Percentage
0-10 11-20 21-30 31-40 41-50 51-60 61-80
Age in years
Graph 1: Showing Age Incidence
141
Table – 3: Sex Incidence
Sex No. of Patients Percentage
Male 15 35.0
Female 25 65.0
In our study of, salivary gland swelling due to various causes, out of 40 cases
15(35%) cases was of male and 25(65%) cases of female.
Graph 2: Showing Sex Incidence
35%
65%
Male
Female
142
Table – 4: Mode of Clinical Presentation
Mode No. of Cases Percentage
Swelling 40 100.0
Pain 26 65.0
Fever 8 20.0
Increased salivation 11 27.5
Tenderness 22 55.0
Fixity of swelling 4 10.0
Ear lobe elevation 19 47.5
Deep lobe involvement 3 7.5
Facial nerve paralysis 1 2.8
In our study, all cases presented with, symptoms of swelling (100%), 65 %
(26) presented with pain. 55 %( 22) presented with tenderness. Three cases were with
deep lobe involvement (11.4%), 19 cases of ear lobe elevation (47.5%). Facial nerve
paralysis occurred in one case (2.8%).
Graph 3: Showing Mode of Clinical Presentation
100
65
2027.5
55
10
47.5
7.52.8
0
20
40
60
80
100
120
Swelling
Pain
Fever
Increased
salivation
Tenderness
Fixity of
swelling
Ear lobe
elevation
Deep lobe
involvement
Facial nerve
paralysis
Percentage
143
Table – 5: Site for Various Salivary Gland Swellings
No. of cases Parotid Submandibular Sublingual
40 25 (62.5%) 12(30.0%) 3(7.5%)
In our study, 62.5% (25 cases) were found in the parotid gland, 30% cases
(12) in submandibular gland and 7.5% cases (3) in the sublingual gland.
62.5
30
7.5
0
10
20
30
40
50
60
70
Percentage
Parotid Submandibular Sublingual
Graph 4: Showing Sites of various Salivary
Swellings
144
Table – 6: Various Causes of Salivary Swelling
Lesions No. of Cases Percentage
Noninflammatory non neoplastic 15 37.5
Neoplastic 25 65.0
Total 40 100.0
In our study, out of 40 cases, neoplastic lesions of 65.0 %( 25 cases) and non
inflammatory non neoplastic lesions of 37.5% (15 cases) were seen.
15
25
0
5
10
15
20
25
Percentage
Noninflammatory non
neoplastic
Neoplastic
Graph 5: Showing Causes of Salivary Swelling
145
Table – 7: Incidence of Non Inflammatory, Non Neoplastic Swellings
Lesions No. of cases Percentage
Sialolithiasis 12 80
Ranula 3 20
In our study, out of 15 cases, 12 (80%) were sialolithiasis and 3 cases (20%)
of sublingual ranula.
80
20
0
10
20
30
40
50
60
70
80
Percentage
Sialolithiasis Ranula
Graph 6: Showing Incidence of Non
Inflammatory, Non Neoplastic Swellings
146
Table – 8: Site Involvement in Non Inflammatory Non Neoplastic Swellings
Parotid Sub mandibular Sublingual
No. of cases
R L R L R L
11 - - (41.66%) 5 (58.33%) 7 3(100%) -
In our study, 41.66% (5) of cases of sialolithiasis were in right submandibular
gland, 58.33%(7) of cases in the left submandibular gland and 3 cases (100%) of
ranula were seen in right sublingual gland only.
0 0
41.66
58.33
100
0
0
10
20
30
40
50
60
70
80
90
100
Percentage
Parotid Submandibular Sublingual
Graph 7: Showing Site Involvement in Non
Inflammatory Non Neoplastic Swellings
Right
Left
147
Table – 9: Incidence of Benign and Malignant Salivary Gland Tumours
Lesions No. of Cases Percentage
Benign 24 96.1
Malignant 1 2.5
In our study, out of 25 salivary tumors, 96.1% were benign and 2.5%
malignant.
96.1
2.5
0
10
20
30
40
50
60
70
80
90
100
Percentage
Benign Malignant
Graph 8: Showing Incidence of Benign and
Malignant Salivary Gland Tumours
148
Table – 10: Site and Side Distribution of Various Salivary Gland Tumours
No. of tumours Parotid Sub Mandibular Sublingual
25 25 - -
R L R L R L
14 (53.84%) 11 (46.15%) - - - -
In our study, all the salivary gland tumors were found in the parotid gland. 14
(53.84%) cases were found in right parotid and 11 (46.15%) cases were found in the
left parotid gland. No case was seen in submandibular and sublingual gland.
5.84
46.15
0 0 0 0
0
5
10
15
20
25
30
35
40
45
50
Percentage
Parotid Submandibular Sublingual
Graph 9: Showing Site and Side Distribution
of Various Salivary Gland Tumours
Right
Left
149
Table – 11: Incidence of Superficial and Deep Lobe Involvement of
Parotid Gland Tumours
No of Tumors Superficial Lobe Deep Lobe
25 22(88.46%) 3(11.53%)
In our study, out of 25 cases of parotid tumors, 22 (88.46%) cases were seen in
superficial and 3 (11.53%) in deep lobe.
Graph 10: Showing Incidence of Superficial and
Deep Lobe Involvement of
Parotid Gland Tumours
Deep Lobe
(88.46%)
Superficial Lobe
(11.53%)
150
Table – 12: Incidence of Various Salivary Glands Tumours
Lesion No. of Cases Percentage
Pleomorphic adenoma 21 84.6
Warthin tumour 3 11.53
Adenoid cystic carcinoma 1 3.8
Total 25 99.93
In our study, out of 25 salivary gland tumors, pleomorphic adenoma was
84.6% (21), 11.53% (3) of Warthin tumour and One case (3.8%) of adenoid cystic
carcinoma.
84.6
11.53
3.8
0
10
20
30
40
50
60
70
80
90
Percentage
Pleomorphic
adenoma
Warthin tumour Adenoid cystic
carcinoma
Graph 11: Showing Incidence of Various
Salivary Glands Tumours
151
Table – 13: Correlation of FNAC and Histopathology
Lesions No. of Patients FNAC (%) BIOPSY (%)
Pleomorphic adenoma 22 100 100
Warthin tumour 3 100 100
Adenoid cystic Ca. 1 - -
In our study, the accuracy of FNAC was 100% in case of benign salivary
gland tumours. One case which was diagnosed by FNAC as adenoid cystic carcinoma
was referred to higher center for the management.
100 100 100 100
0 0
0
10
20
30
40
50
60
70
80
90
100
Percentage
Pleomorphic
adenoma
Warthin tumour Adenoid cystic
Ca.
Graph 12: Showing Correlation of FNAC and
Histopathology
FNAC
Biopsy
152
Table – 14: Surgical Procedures Adopted for Various Salivary Gland Swellings
Procedures No. of Patients Percentage
Excision of submandibular gland 12 28.20
Superficial parotidectomy 21 56.41
Total Parotidectomy 3 7.6
Excision ranula 3 7.6
Total 39 100
In our study, surgery was the treatment for all cases of tumors. Superficial
parotidectomy was done in all the 21 cases of parotid tumour (56.41%) without deep
lobe involvement and total parotidectomy was done in 3 cases (7.6%) with deep lobe
involvement. In all the cases of submandibular gland lesions, excision of
submandibular gland was done. Excision of the sublingual gland was done in 3 cases
of ranula. One case of adenoid cystic cacinoma was referred to higher center because
of the advanced malignancy.
28.2
56.41
7.67.6
0
10
20
30
40
50
60
Percentage
Excision of
submandibular
gland
Superficial
parotidectomy
Total
Parotidectomy
Excision ranula
Graph 13: Showing Surgical Procedures Adopted for
Various Salivary Gland Swellings
153
Table– 15: Post Operative Complications
Nature of Complications No. of Patients Percentage
Facial nerve paralysis 1 2.5
Mandibular nerve paralysis 1 2.5
Wound infection 8 20
Post operative complications in my study of 40 cases were low. One case of
facial nerve paralysis occured after parotid tumour surgery in the case of deep lobe
involvement and one case of mandibular nerve palsy occured with submandibular
sialadenectomy, wound infection was noticed in 8 cases.
Graph 14: Showing Post Operative Complications
20
2.5
2.5
Facial nerve paralysis Mandibular nerve paralysis Wound infection
154
DISCUSSION
Comparison of our present series of 40 cases with various series of other
authors.
Table – 16: Incidence Per Year Of Salivary Gland Tumours In Different Series
Series No. of
tumours
Period of
study
No. of cases per
year
Potdaretar12o
1969 188 10 18
Gupta et al121
1975 113 21 05
Khazanchi et al122
1988 88 6 15
Fennetal123
1982 57 15 04
Renehan et al123
1996 1194 45 27
Present study 25 2 13
In our series, mean incidence is 13 cases per year. This incidence correlates
with most of studies by other authors in the above data.
Table – 17: Incidence Of Sialolithiasis In Various Studies
Series No. of cases Parotid Sub mandibular Sub lingual
Antognini et al125
1971 396 8.3 91.4 0.3
Pizzirani et al126
1985 102 7.8 92.2 -
J. Lustmann et al127
1990 245 4.5 94.3 0.4
Present study 12 - 100 -
In our study, incidence percentage of sialolithiasis i.e., 12 cases were found in
submandibular gland which co-relates with most of the authors in the above table
series.
155
Table – 18: Frequency of Benign And Malignant Salivary Tumours In Different
Series
Series
No. Of
tumors
Benign Malignant
Foote et al128
1954 730 68.30% 31.70%
Skolniketal129
1977 435 59.40% 30.60%
Khazanchi et al122
1988 88 63.60% 36.40%
Renehan et al124
1996 1194 80.00% 0.00%
Present study 25 97.5% 2.5%
In accordance with the observation in other series, the benign tumors
predominate in our study.
Table – 19: Location of Various Tumours in Different Series
Series Parotid Submandibular Sublingual
Budhraja et al130
1974 82.10% 12.40% 5.5%
Sharkey F.E. et al131
1977 80.50% 6.00% 9.0%
Everson et al67 1985 72.90% 10.70% 16.4%
Renehan et al124
1996 91.00% 4.0% 5%
Present study 100% - -
In our study, all the salivary gland tumors were observed in parotid gland.
Comparative study was in accordance to Renehan et al. Tumours of sublingual glands
156
are extremely rare and no cases were recorded with submandibular gland, because of,
small number of cases and short study period.
Table – 20: Incidence of Superficial and Deep Lobe Involvement of Parotid
Gland Tumours in Different Series
Series
Total No. of
cases
Superficial Deep
H. Leverstein et al., 1997132
245 192(78.3%) 54(22%)
H. Laccourreve et al.,133
1994
229 118(51.5%) 111 (48.4%)
Present Series 25 22(88.46%) 3(11.53%)
In our study, out of 25 parotid tumours, 22 (88.46%) were seen in superficial
lobe of parotid and 3 (11.53%) in deep lobe which is in accordance with the H.
Leverstein et al., series.
Table – 21: Average Age Incidence of Salivary Gland Tumours in Different
Series
Average age in years
SERIES
Benign Malignant
Potdar etal120
1969 40 49
Budhrajetal130
1974 41 41
Skolnik et al129
1977 45 56
Khazanchi et al122
1988 44 50
Renehan et al124
1996 55 59
Present study 47 80
157
In our series of salivary gland tumors out of 25 cases, 24 cases were benign
with mean age 45 and one case was malignant of 80 years age.
The results observed in our study are consistent with other studies shown in
the table.
In our study of 40 cases of salivary gland swelling, shows that, surgery is the
treatment of choice in all cases of salivary gland swellings. FNAC plays an important
role in the diagnosis of salivary gland tumors and accuracy rate was 100% in our
series.
In our study, there was no recurrence and nil mortality.
Benign swelling of the salivary gland found in lower decade of life, where as,
malignant swelling was found in 8th decade of life, which correlates with many
authors in other series.
Table – 22: FNAC Comparison with Pathologic Diagnosis
In Different Series
Series Benign Malignant
Frable and Frable 1982134
91% 92%
Spiro RH et al., 1974135
98% 93%
Present Study 100% 100%
In our study of 40 cases, FNAC was in accordance with the other author's
series shown in above table.
158
CONCLUSION
Following the study of 40 cases of salivary gland swellings, the following
conclusions can be made.
� Diagnosis of the salivary gland tumors must be considered in any patient
presenting with salivary gland swelling
� Salivary gland swelling occur more commonly in 3rd and 4
th decades of life and
seen most common in females
� Neoplastic salivary gland swellings were more common than non inflammatory
swellings.
� Sialolithiasis is the predominant non inflammatory swelling.
� Sialolithiasis occur more commonly in the submandibular salivary glands.
� Salivary gland tumors occur more commonly in the parotid gland, most often
benign, pleomorphic adenoma constitute majority of all neoplasm
� Swelling is the commonest symptom. The fact that the mass has been present for
several years is no guarantee that it is benign.
� History and physical examination complement FNAC and help in diagnosis.
FNAC has good accuracy in diagnosing salivary gland swellings.
� Surgery is the main modality of treatment in salivary gland sialolithiasis. Most
commonly done surgery is excision of submandibular salivary gland and also for
salivary gland tumors. Most commonly done surgery is superficial parotidectomy.
� Long term follow up is necessary as salivary gland tumors tend to occur after long
period of time
159
� Since most malignant tumors is asymptomatic and long standing benign tumors
can undergo malignant change, community awareness and early referral is
necessary, as prognosis is good if treated early.
160
SUMMARY
� The clinical material in this study includes the details of 40 cases of salivary gland
swellings admitted in Chigateri general hospital and J.J.M. Medical College,
Davangere during the period of June 2009 to July 2011.
� The incidence of salivary gland swellings is highest in the 3rd and 4
th decade of
life. Benign tumors were more common in 20 -50 years and malignancy was seen
in one patient of age 80 years.
� In this series, 14 patients were male(35%) and 26(65%) patients were female.
With male to female ratio of 1:1.8
� Commonest of salivary swellings was seen in parotid gland with 25 cases (62.5%)
� In this series, 15 cases (37.5 %) of salivary swellings was due to non-
inflammatory and non-neoplastic swellings and 25 cases (65%) was due to
neoplatic swellings
� Incidence of non-inflammatory non neoplastic swellings was most often seen in
submandibular salivary glands. 80 % were seen affecting the submandibular gland
and 20 % was seen affecting the sublingual glands.
� Incidence of tumours was highest in the parotid. Incidence of benign tumours is
96.1% and malignant tumors are 2.5%. pleomorphic adenoma is the commonest
benign tumour and adenoid cystic carcinoma was the only malignant tumour
� Patients presented with history of swellings varying from 15 days to 5 years.
Swelling is the most common symptom. Pain was the second most common
symptoms. Pain was noticed in 65% of the cases. And tenderness was noticed in
55% of the cases.
� Patient with malignant tumor had other symptoms in addition to the swelling, like
pain, facial asymmetry due to facial nerve paresis.
161
� Final diagnosis was arrived at by Physical examination and FNAC. FNAC is the
reliable and sensitive tool for diagnosing salivary gland tumours. There was an
overall diagnostic accuracy of 100%
� Surgery is the treatment in all the cases of salivary swelling except one case i.e.,
adenoid cystic carcinoma was referred to higher centre. Out of 25 cases of parotid
tumour. Superficial parotidectomy was done in 21 cases( 56.4%) and total
parotidectomy for 3 cases (7.6%) . For all the submandibular gland lesions
sialadenectomy was done. Sublingual gland excision was carried out for 3 cases of
ranula.
� Wound infection was the major complication with 8 cases and one case of facial
nerve paralysis (2.1%) was observed in case of total parotidectomy and one case
of mandibular nerve palsy (2.1%) occurred in one case of sialadentectomy.
� Out of 40 cases, 15 cases (37.5%) were due to non-inflammatory and non-
neoplastic swellings. Out of which 12 cases (80%) was due to submandibular
sialoloithiasis and 3 cases (20%) was due to ranula of the sublingual glands.25
Cases (65%) were due to salivary gland tumours. Out of which Pleomorphic
adenoma is seen in 21 cases (84.6%), Warthin’s tumour is seen in 3 cases
(11.53%) and one case of adenoid cystic carcinoma (3.8%)
� With proper diagnosis and appropriate treatment. Salivary gland swelling can be
cured with almost 100%.
� Successful management of the salivary gland neoplasm depends on accurate
clinical assessment and diagnosis, with appropriate use of fine needle aspiration
and CT or MR imaging. Moreover, knowledge of the particular behaviour of each
tumor type guides the development of an appropriate treatment plan for each
individual patient.
162
� Prognosis is good in benign as well as malignant tumors of salivary glands, if
treated early.
� There was no mortality in our study of 40 cases after follow up for 6 months to 2
years. But follow up period was inadequate as salivary gland tumours are known
for their late recurrence. The adequacy of treatment cannot be commented because
of short period of follow up.
� The study group in this series is small, as compared to large series in western
literature. So statistical data in this series may not represent the actual data quoted
in western literature.
163
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176
ANNEXURE -1
PROFORMA
NAME : DATE OF ADMISSION :
AGE : DATE OF OPERATION :
OCCUPATION: DATE OF DISCHARGE :
ADDRESS: I.P. No.:
INCOME :
PROVISIONAL DIAGNOSIS:
COMPLAINTS WITH DURATION:
HISTORY OF PRESENT ILLNESS:
• Swelling
- Onset
- Site
- Duration
- Rate of growth
- Pain
- Relation to food
• Ulceration and discharge
• H/o Fever
• H/o dryness of Mouth
• H/o Trauma
• H/o Difficulty in the movement of jaw
• H/o Any other swelling in the opposite side
• H/o Appetite and weight
PAST HISTORY:
H/o any similar complaints in the past
H/o collagen disease
FAMILY HISTORY:
H/o salivary gland enlargement in the family
H/o Diabetes, Hypertension, Collagen disease etc.
177
PERSONAL HISTORY: DIET APPETITE SLEEP
BOWEL MICTURITION
SMOKING CHEWING ALCOHOLIC
GENERAL PHYSICAL EXAMINATION:
BUILT NOURISHMENT PALLOR
CYANOSIS JAUNDICE CLUBBING
GENERALISED LYMPHADENOPATHY
TEMP: PULSE: RESP. RATE : B. P. :
LOCAL EXAMINATION:
INSPECTION:
- Number
- Site
- Shape
- Size
- Surface
- Borders
- Skin over the swelling
- Ear Lobule raised/not raised
- Fistula and its position over the gland or duct
- Movements of the jaw
PALPATION:
- Temperature
- Tenderness
- Size, Shape
- Extent
- Surface, Borders
- Fistula
- Mobility
- Fixity to overlying skin
- Relation to masseter muscle
- Plane of the swelling
178
- Jaw movements
- Facial and lingual nerve palsy
- Regional lymph nodes
INTRAORAL EXAMINATION:
- Oral Hygiene Caries Tooth Sepsis
- (Cleaning material used)
- (Whether gargling after each meal)
- Bulging or fullness in the floor of the mouth or in the
- Supra-tonsillar region. Opening of the parotid duct
- Opening of the Wharton's duct
- Bi-digital examination
- Any other swelling in the oral cavity
SYSTEMIC EXAMINATION:
- Cardiovascular system
- Respiratory system
- GIT Liver
- Genitourinary system
- CNS
- Bones
INVESTIGATIONS:
- Hb% TC DC ESR
- Blood Sugar Blood Urea Serum Creatinine
- Urine: Albumin Sugar: Microscopy:
- X-ray chest/Screening chest
- X-ray mandible
- Sialography
- Radio-Isotope Scan
- FNAC
CLINICAL DIAGNOSIS:
179
TREATMENT - Surgical/radiotherapy/Chemotherapy/Survey +
Radiotherapy
SURGICAL
Pre -operative treatment
Type of operation
Findings at operation
Post- Operative period- Wound infection, Fistula,
Facial paralysis,
Any other
BIOPSY REPORT:
FOLLOW-UP:
180
ANNEXURE – II
MASTER CHART
181
182
KEY TO MASTER CHARTS
OCC Occupation
Durn Duration
h\o History of
Sali Salivation
GL invol Gland Involved
T Tenderness
C Consistency
M Mobility
R Right
L Left
IP NO In patient number
H.W House Wife
STU Student
Agri agriculturist
F.N.PAR Facial nerve paralysis
REL Raised Ear Lobule
SKIN CH Skin Changes
D. OPEN Duct open
ROC Radio Opaque Calcification
D. PAR Deep Parotid gland
SIALO Sialography
FNAC Fine Needle Aspiration Cytology
C. DIAGNO Clinical Diagnosis
SUR Surgery
183
HPE Histopathology
N Normal
F Firm
S Soft
H Hard
PR Parotid
SMD Submandibular Gland
SL Sublingual gland
PLA Pleomorphic Adenoma
SUP.PARO Superficial Parotidectomy
TOT-PARO Total Parotidectomy
SMD .EX Sub-Mandibular gland excision
X RAY MND X- RAY Mandible
ACA.PR Adeno Carcinoma Parotid
WT.PR Warthin’s tumour parotid
SMD. SIAL Submandibular Sialolithiasis
SMD. EX Submandibiular Excision
184
ANNEXURE- III
CONSENT FORM
FOR OPERATION/ANAESTHESIA
I _____________________ Hosp. No. __________________in my full senses
hereby give my complete consent for ____________________________ or any other
procedure deemed fit which is a / and diagnostic procedure / biopsy / transfusion /
operation to be performed on me / my son / my daughter / my ward ____________
age _____________under any anaesthesia deemed fit. The nature and risks involved
in the procedure have been explained to me to my satisfaction. For academic and
scientific purpose the operation/procedure may be televised or photographed.
Date :
Signature/Thumb Impression
of Patient/Guardian
Name :
Designation:
Guardian
Relationship
Full Address